Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of monoamine oxidase type A (MAO-A) by clorgyline (4 mg/kg i.p.), MAO-B by (-)deprenyl (1 mg/kg i.p.), both MAO-A and MAO-B by nialamide (75 mg/kg i.p.) or peripheral neuronal << MAO >> by [[ debrisoquin ]] (40 mg/kg i.p.).


Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of << monoamine oxidase type A >> (MAO-A) by [[ clorgyline ]] (4 mg/kg i.p.), MAO-B by (-)deprenyl (1 mg/kg i.p.), both MAO-A and MAO-B by nialamide (75 mg/kg i.p.) or peripheral neuronal MAO by debrisoquin (40 mg/kg i.p.).


Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of monoamine oxidase type A (<< MAO-A >>) by [[ clorgyline ]] (4 mg/kg i.p.), MAO-B by (-)deprenyl (1 mg/kg i.p.), both MAO-A and MAO-B by nialamide (75 mg/kg i.p.) or peripheral neuronal MAO by debrisoquin (40 mg/kg i.p.).


The results suggest that most of the << HVA >> in plasma is derived from deamination of DA by [[ MAO-A ]] in peripheral neurons; that DOPAC in plasma is derived from cells outside the central nervous system; that DHPG in plasma is derived virtually exclusively from the metabolism of norepinephrine in sympathetic nerve endings and that residual levels of HVA after treatment with debrisoquin provide an improved but limited indication of central dopaminergic activity.


The results suggest that most of the HVA in plasma is derived from deamination of << DA >> by [[ MAO-A ]] in peripheral neurons; that DOPAC in plasma is derived from cells outside the central nervous system; that DHPG in plasma is derived virtually exclusively from the metabolism of norepinephrine in sympathetic nerve endings and that residual levels of HVA after treatment with debrisoquin provide an improved but limited indication of central dopaminergic activity.


After << loperamide >> administration ACTH levels fell to a nadir of 135 +/- 76 pg/ml, and then CRH was still able to induce an [[ ACTH ]] increase; the pattern of ACTH response to CRH was slightly delayed.


After << loperamide >> administration [[ ACTH ]] levels fell to a nadir of 135 +/- 76 pg/ml, and then CRH was still able to induce an ACTH increase; the pattern of ACTH response to CRH was slightly delayed.


<< Ambenonium >> is known to be an inhibitor of [[ acetylcholinesterase ]], and recent data have shown this drug to antagonize muscarinic receptors as well.


<< Ambenonium >> is known to be an inhibitor of acetylcholinesterase, and recent data have shown this drug to antagonize [[ muscarinic receptors ]] as well.


Ambenonium was a less potent antagonist of tissue responses to acetylcholine, and the underestimation in the pKB (as compared to that obtained with bethanechol) could be eliminated by prior treatment of tissues with the << acetylcholinesterase >> inhibitor [[ neostigmine ]].


These data suggested that << ambenonium >> had a dual effect on tissue responses to acetylcholine-producing potentiation by blockade of [[ acetylcholinesterase ]] and concomitant antagonism by blockade of muscarinic receptors.


These data suggested that << ambenonium >> had a dual effect on tissue responses to acetylcholine-producing potentiation by blockade of acetylcholinesterase and concomitant antagonism by blockade of [[ muscarinic receptors ]].


These data suggested that ambenonium had a dual effect on tissue responses to << acetylcholine >>-producing potentiation by blockade of [[ acetylcholinesterase ]] and concomitant antagonism by blockade of muscarinic receptors.


However, << betaxolol >> produces less systemic beta 2- and possibly [[ beta 1-adrenergic receptor ]] blockade than either timolol or levobunolol.


However, betaxolol produces less systemic beta 2- and possibly << beta 1-adrenergic receptor >> blockade than either [[ timolol ]] or levobunolol.


However, betaxolol produces less systemic beta 2- and possibly << beta 1-adrenergic receptor >> blockade than either timolol or [[ levobunolol ]].


<< Tyrosinase >> catalyzes an unusual oxidative decarboxylation of [[ 3,4-dihydroxymandelate ]].


<< Tyrosinase >> usually catalyzes the conversion of [[ monophenols ]] to o-diphenols and oxidation of diphenols to the corresponding quinones.


<< Tyrosinase >> usually catalyzes the conversion of monophenols to o-diphenols and oxidation of [[ diphenols ]] to the corresponding quinones.


<< Phenol oxidase >> inhibitors such as [[ phenylthiourea ]], potassium cyanide, and sodium azide inhibited the reaction drastically, suggesting the participation of the active site copper of the enzyme in the catalysis.


<< Phenol oxidase >> inhibitors such as phenylthiourea, [[ potassium cyanide ]], and sodium azide inhibited the reaction drastically, suggesting the participation of the active site copper of the enzyme in the catalysis.


<< Phenol oxidase >> inhibitors such as phenylthiourea, potassium cyanide, and [[ sodium azide ]] inhibited the reaction drastically, suggesting the participation of the active site copper of the enzyme in the catalysis.


<< Mimosine >>, a well-known competitive inhibitor of [[ tyrosinase ]], competitively inhibited the new reaction also.


Present studies demonstrate that << mushroom tyrosinase >> will also catalyze [[ quinone methide ]] production with the same active site copper if a suitable substrate such as 3,4-dihydroxymandelic acid is provided.


Present studies demonstrate that << mushroom tyrosinase >> will also catalyze quinone methide production with the same active site copper if a suitable substrate such as [[ 3,4-dihydroxymandelic acid ]] is provided.


The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (<< t-PA >>) is inhibited by Cl-, at physiological concentrations, and stimulated by [[ epsilon-aminocaproic acid ]] (EACA), as well as fibrin(ogen).


The activation of << human [Glu1]plasminogen >> [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by [[ epsilon-aminocaproic acid ]] (EACA), as well as fibrin(ogen).


The activation of human [Glu1]plasminogen [<< ( Glu1]Pg >>) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by [[ epsilon-aminocaproic acid ]] (EACA), as well as fibrin(ogen).


The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain << tissue plasminogen activator >> (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by [[ epsilon-aminocaproic acid ]] (EACA), as well as fibrin(ogen).


The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (<< t-PA >>) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid ([[ EACA ]]), as well as fibrin(ogen).


The activation of << human [Glu1]plasminogen >> [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid ([[ EACA ]]), as well as fibrin(ogen).


The activation of human [Glu1]plasminogen [<< ( Glu1]Pg >>) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid ([[ EACA ]]), as well as fibrin(ogen).


The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain << tissue plasminogen activator >> (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid ([[ EACA ]]), as well as fibrin(ogen).


The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (<< t-PA >>) is inhibited by [[ Cl- ]], at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen).


The activation of << human [Glu1]plasminogen >> [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by [[ Cl- ]], at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen).


The activation of human [Glu1]plasminogen [<< ( Glu1]Pg >>) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by [[ Cl- ]], at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen).


The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain << tissue plasminogen activator >> (t-PA) is inhibited by [[ Cl- ]], at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen).


The presence of << Cl- >> inhibits the stimulation of [[ [Glu1]Pg ]] activation that would normally occur in the presence of fibrinogen, a result of possible importance to the observation that some degree of systemic fibrinogenolysis accompanies therapeutic use of tissue plasminogen activator.


Sodium-dependent << norepinephrine >>-induced currents in [[ norepinephrine-transporter ]]-transfected HEK-293 cells blocked by cocaine and antidepressants.


Sodium-dependent norepinephrine-induced currents in << norepinephrine-transporter >>-transfected HEK-293 cells blocked by [[ cocaine ]] and antidepressants.


Whole-cell voltage-clamp of << hNET >>-293 cells reveals [[ NE ]]-induced, Na(+)-dependent currents blocked by antidepressants and cocaine that are absent in parental cells.


Whole-cell voltage-clamp of << hNET >>-293 cells reveals NE-induced, Na(+)-dependent currents blocked by antidepressants and [[ cocaine ]] that are absent in parental cells.


To explain our observations, we propose that << hNETs >> function as ion-gated ligand channels with an indefinite stoichiometry relating ion flux to [[ NE ]] transport.


BACKGROUND: The active metabolite of the anti-inflammatory drug << nabumetone >> has been characterized as a selective inhibitor of the inducible [[ prostaglandin H synthase ]] (PGHS).


BACKGROUND: The active metabolite of the anti-inflammatory drug << nabumetone >> has been characterized as a selective inhibitor of the inducible prostaglandin H synthase ([[ PGHS ]]).


Moreover, the production of << TXB2 >> during whole blood clotting was assessed as an index of the [[ cyclooxygenase ]] activity of platelet PGHS-1 ex vivo.


Moreover, the production of << TXB2 >> during whole blood clotting was assessed as an index of the cyclooxygenase activity of platelet [[ PGHS-1 ]] ex vivo.


The daily administration of low-dose << aspirin >> (40 mg), a selective inhibitor of platelet [[ PGHS-1 ]], caused a cumulative inhibition of urinary 11-dehydro-TXB2 and whole blood TXB2 production that recovered with a timecourse consistent with platelet turnover.


The daily administration of low-dose aspirin (40 mg), a selective inhibitor of platelet << PGHS-1 >>, caused a cumulative inhibition of urinary [[ 11-dehydro-TXB2 ]] and whole blood TXB2 production that recovered with a timecourse consistent with platelet turnover.


The daily administration of low-dose aspirin (40 mg), a selective inhibitor of platelet << PGHS-1 >>, caused a cumulative inhibition of urinary 11-dehydro-TXB2 and whole blood [[ TXB2 ]] production that recovered with a timecourse consistent with platelet turnover.


CONCLUSIONS: << Nabumetone >> does dose-dependently inhibit the [[ cyclooxygenase ]] activity of platelet PGHS-1 of healthy subjects both in vivo and ex vivo.


CONCLUSIONS: << Nabumetone >> does dose-dependently inhibit the cyclooxygenase activity of platelet [[ PGHS-1 ]] of healthy subjects both in vivo and ex vivo.


Preclinical efficacy of << emedastine >>, a potent, selective [[ histamine H1 ]] antagonist for topical ocular use.


(2) Exposure histories vary in secondary 11q23 leukemia, as the only << topoisomerase II >> inhibitor was [[ dactinomycin ]] in one case, and, in another case, no topoisomerase II inhibitor was administered.


<< Indomethacin >>, piroxicam, and sulindac sulfide were found to preferentially inhibit [[ PGHS-1 ]].


Indomethacin, << piroxicam >>, and sulindac sulfide were found to preferentially inhibit [[ PGHS-1 ]].


Indomethacin, piroxicam, and << sulindac sulfide >> were found to preferentially inhibit [[ PGHS-1 ]].


<< 6-Methoxy-2-naphthylacetic acid >>, the active metabolite of Relafen, inhibits murine [[ PGHS-2 ]] preferentially.


6-Methoxy-2-naphthylacetic acid, the active metabolite of << Relafen >>, inhibits murine [[ PGHS-2 ]] preferentially.


<< Aspirin >> irreversibly inhibits [[ PGHS-1 ]], preventing this isozyme from forming PGH2 or any other oxygenated product; in contrast, aspirin treatment of PGHS-2 causes this enzyme to form 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid (15-HETE) instead of PGH2.


Aspirin irreversibly inhibits PGHS-1, preventing this isozyme from forming PGH2 or any other oxygenated product; in contrast, aspirin treatment of << PGHS-2 >> causes this enzyme to form 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid ([[ 15-HETE ]]) instead of PGH2.


Aspirin irreversibly inhibits PGHS-1, preventing this isozyme from forming PGH2 or any other oxygenated product; in contrast, aspirin treatment of << PGHS-2 >> causes this enzyme to form [[ 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid ]] (15-HETE) instead of PGH2.


Anorexia induced by (+)-amphetamine, phentermine, diethylpropion and phenylpropanolamine seems to be the result of their ability to increase the release of noradrenaline and/or dopamine from nerve terminals and inhibit their reuptake or, in the case of << phenylpropanolamine >>, to stimulate directly [[ alpha 1-adrenoceptors ]].


Under these conditions, blockade of << monoamine oxidase >> with [[ pargyline ]] (100 microM for 15 min) caused a leftward displacement of concentration-effect curves for both 5-methoxytryptamine (5-MeO-T) and tryptamine.


In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including 1-m-chlorophenylpiperazine (m-CPP), [[ Ru 24969 ]], MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including 1-m-chlorophenylpiperazine (m-CPP), [[ Ru 24969 ]], MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including 1-m-chlorophenylpiperazine (m-CPP), Ru 24969, [[ MK 212 ]] and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including 1-m-chlorophenylpiperazine (m-CPP), Ru 24969, [[ MK 212 ]] and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including 1-m-chlorophenylpiperazine (m-CPP), Ru 24969, MK 212 and [[ SCH 23390 ]] were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including 1-m-chlorophenylpiperazine (m-CPP), Ru 24969, MK 212 and [[ SCH 23390 ]] were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including [[ 1-m-chlorophenylpiperazine ]] (m-CPP), Ru 24969, MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including [[ 1-m-chlorophenylpiperazine ]] (m-CPP), Ru 24969, MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including 1-m-chlorophenylpiperazine ([[ m-CPP ]]), Ru 24969, MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including 1-m-chlorophenylpiperazine ([[ m-CPP ]]), Ru 24969, MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.


Phorbol esters and << norepinephrine >> destabilize [[ alpha 1B-adrenergic receptor ]] mRNA in vascular smooth muscle cells.


The mechanism by which << norepinephrine >> (NE) down-regulates [[ alpha 1B-adrenergic receptor ]] (alpha-AR) mRNA was studied in rabbit aortic smooth muscle cells.


The mechanism by which << norepinephrine >> (NE) down-regulates alpha 1B-adrenergic receptor ([[ alpha-AR ]]) mRNA was studied in rabbit aortic smooth muscle cells.


The mechanism by which norepinephrine (<< NE >>) down-regulates [[ alpha 1B-adrenergic receptor ]] (alpha-AR) mRNA was studied in rabbit aortic smooth muscle cells.


The mechanism by which norepinephrine (<< NE >>) down-regulates alpha 1B-adrenergic receptor ([[ alpha-AR ]]) mRNA was studied in rabbit aortic smooth muscle cells.


<< NE >>, phorbol esters, and bradykinin each decreased [[ alpha-AR ]] mRNA levels by 70-80%.


NE, << phorbol esters >>, and bradykinin each decreased [[ alpha-AR ]] mRNA levels by 70-80%.


The << protein kinase C >> inhibitor [[ (+)-1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride ]] (H-7) abolished the effects of phorbol esters and NE and decreased basal mRNA levels by 52 +/- 3%.


The << protein kinase C >> inhibitor (+)-1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride ([[ H-7 ]]) abolished the effects of phorbol esters and NE and decreased basal mRNA levels by 52 +/- 3%.


Neither ryanodine nor << EGTA >> inhibited down-regulation of [[ alpha-AR ]] mRNA by NE.


Neither << ryanodine >> nor EGTA inhibited down-regulation of [[ alpha-AR ]] mRNA by NE.


Neither ryanodine nor EGTA inhibited down-regulation of << alpha-AR >> mRNA by [[ NE ]].


<< Actinomycin D >> caused [[ alpha-AR ]] mRNA level to decrease with a half-life of 3.2 +/- 0.4 h and blocked the effect of H-7 to decrease basal alpha-AR mRNA level.


<< Actinomycin D >> caused alpha-AR mRNA level to decrease with a half-life of 3.2 +/- 0.4 h and blocked the effect of H-7 to decrease basal [[ alpha-AR ]] mRNA level.


Both << NE >> and phorbol esters increased the rate of [[ alpha-AR ]] mRNA degradation.


Both NE and << phorbol esters >> increased the rate of [[ alpha-AR ]] mRNA degradation.


In << NE >>-desensitized cells, phorbol esters and bradykinin each caused the expected down-regulation of [[ alpha-AR ]] mRNA.


In NE-desensitized cells, << phorbol esters >> and bradykinin each caused the expected down-regulation of [[ alpha-AR ]] mRNA.


The << protein phosphatase >> inhibitor [[ okadaic acid ]] prolonged the normally transient effect of NE for at least 24 h.


The specific binding is displaced by the selective << 5-HT1D >> agonist [[ sumatriptan ]] but not by the mixed 5-HT1A/1D agonist 5-carboxyamidotryptamine.


HeLa cells transfected with the MR77 gene exhibited inhibition of << adenylate cyclase >> in response to [[ serotonin ]].


The antiarrhythmic effects of exogenous adenosine and Valsalva on this form of VT may be due to receptor-mediated inhibition of adenylate cyclase or to noncardiac receptor-mediated effects, i.e., exogenous << adenosine >> may modulate VT through alterations in autonomic tone by activation of arterial [[ chemoreceptors ]], and Valsalva has been shown to decrease venous return, resulting in a reduction in cardiac dimensions and myocardial stretch.


VT recurred with the addition of << aminophylline >>, a competitive [[ adenosine A1-receptor ]] antagonist.


Edrophonium (10 mg i.v.), a cholinesterase inhibitor that potentiates the effects of acetylcholine at the << muscarinic cholinergic receptor >>, terminated VT in four of four patients, an effect that was reversed by [[ atropine ]].


<< Edrophonium >> (10 mg i.v.), a [[ cholinesterase ]] inhibitor that potentiates the effects of acetylcholine at the muscarinic cholinergic receptor, terminated VT in four of four patients, an effect that was reversed by atropine.


<< Amantadine >> induces [[ c-fos ]] in rat striatum: reversal with dopamine D1 and NMDA receptor antagonists.


<< Amantadine >> (1-aminoadamantane) induced [[ Fos ]] expression in the central, dorsal-medial and ventral-medial part of the striatum.


Amantadine (<< 1-aminoadamantane >>) induced [[ Fos ]] expression in the central, dorsal-medial and ventral-medial part of the striatum.


The distribution pattern of << Fos >> induced by [[ amantadine ]] was more similar to those seen with dopaminomimetics than with N-methyl-D-aspartate (NMDA) receptor antagonists.


Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the NMDA receptor antagonist, MK-801, blocked << amantadine >> induction of [[ Fos ]] in the striatum.


Pretreatment with the dopamine D1 receptor antagonist, << SCH23390 >>, and the NMDA receptor antagonist, MK-801, blocked amantadine induction of [[ Fos ]] in the striatum.


Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the NMDA receptor antagonist, << MK-801 >>, blocked amantadine induction of [[ Fos ]] in the striatum.


Pretreatment with the << dopamine D1 receptor >> antagonist, [[ SCH23390 ]], and the NMDA receptor antagonist, MK-801, blocked amantadine induction of Fos in the striatum.


Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the << NMDA receptor >> antagonist, [[ MK-801 ]], blocked amantadine induction of Fos in the striatum.


However, << amantadine >> induction of [[ Fos ]] in the striatum was unaffected by the dopamine D2 receptor antagonist, sulpiride.


However, amantadine induction of Fos in the striatum was unaffected by the << dopamine D2 receptor >> antagonist, [[ sulpiride ]].


These results suggest that << amantadine >> induction of [[ Fos ]] in the rat striatum is related to dopamine D1 and NMDA receptors.


After CFVs were observed for 30 min, the animals were randomly divided in four groups: 5 animals received via a small catheter (26G) placed proximally to the stenosis, an intra-arterial infusion of human recombinant FVIIai (0.1 mg/kg/min for 10 min); 9 animals received AP-1, a monoclonal antibody against rabbit TF (0.1 mg/kg i.v. bolus); 7 animals received ridogrel, a dual thromboxane A2 synthetase inhibitor and thromboxane A2 receptor antagonist (10 mg/kg i.v. bolus); finally, 8 rabbits received << aurintrycarboxilic acid >> (ATA), an inhibitor of platelet [[ glycoprotein Ib ]]/von Willebrand factor interaction (10 mg/kg i.v. bolus).


After CFVs were observed for 30 min, the animals were randomly divided in four groups: 5 animals received via a small catheter (26G) placed proximally to the stenosis, an intra-arterial infusion of human recombinant FVIIai (0.1 mg/kg/min for 10 min); 9 animals received AP-1, a monoclonal antibody against rabbit TF (0.1 mg/kg i.v. bolus); 7 animals received ridogrel, a dual thromboxane A2 synthetase inhibitor and thromboxane A2 receptor antagonist (10 mg/kg i.v. bolus); finally, 8 rabbits received << aurintrycarboxilic acid >> (ATA), an inhibitor of platelet glycoprotein Ib/[[ von Willebrand factor ]] interaction (10 mg/kg i.v. bolus).


After CFVs were observed for 30 min, the animals were randomly divided in four groups: 5 animals received via a small catheter (26G) placed proximally to the stenosis, an intra-arterial infusion of human recombinant FVIIai (0.1 mg/kg/min for 10 min); 9 animals received AP-1, a monoclonal antibody against rabbit TF (0.1 mg/kg i.v. bolus); 7 animals received ridogrel, a dual thromboxane A2 synthetase inhibitor and thromboxane A2 receptor antagonist (10 mg/kg i.v. bolus); finally, 8 rabbits received aurintrycarboxilic acid (<< ATA >>), an inhibitor of platelet [[ glycoprotein Ib ]]/von Willebrand factor interaction (10 mg/kg i.v. bolus).


After CFVs were observed for 30 min, the animals were randomly divided in four groups: 5 animals received via a small catheter (26G) placed proximally to the stenosis, an intra-arterial infusion of human recombinant FVIIai (0.1 mg/kg/min for 10 min); 9 animals received AP-1, a monoclonal antibody against rabbit TF (0.1 mg/kg i.v. bolus); 7 animals received ridogrel, a dual thromboxane A2 synthetase inhibitor and thromboxane A2 receptor antagonist (10 mg/kg i.v. bolus); finally, 8 rabbits received aurintrycarboxilic acid (<< ATA >>), an inhibitor of platelet glycoprotein Ib/[[ von Willebrand factor ]] interaction (10 mg/kg i.v. bolus).


These events are stimulated by NE and by guanethidine, an << hNET >> substrate, and they are blocked by [[ cocaine ]] and the antidepressant desipramine.


These events are stimulated by NE and by guanethidine, an << hNET >> substrate, and they are blocked by cocaine and the antidepressant [[ desipramine ]].


These events are stimulated by << NE >> and by guanethidine, an [[ hNET ]] substrate, and they are blocked by cocaine and the antidepressant desipramine.


These events are stimulated by NE and by << guanethidine >>, an [[ hNET ]] substrate, and they are blocked by cocaine and the antidepressant desipramine.


Voltage-clamp data combined with << NE >> uptake data from these same cells indicate that [[ hNETs ]] have two functional modes of conduction: a classical transporter mode (T-mode) and a novel channel mode (C-mode).


In extending these initial findings, we have shown that cardiac fibrosis (i) is not reversed by correction of mineralocorticoid-induced hypokalemia; (ii) appears not to involve the plasma or tissue renin-angiotensin systems, as fibrosis is largely unaffected by concurrent administration of Losartan or Perindopril; (iii) is independent of cardiac hypertrophy, in that it is equally seen in right and left ventricles, and in rats rendered hypertensive without cardiac hypertrophy by the administration of 9 alpha-fluorocortisol; (iv) is independent of elevated blood pressure, in that it is found in normotensive animals infused peripherally with aldosterone and intracerebroventricularly with the << mineralocorticoid receptor >> (MR) antagonist [[ RU28318 ]]; (v) is via classical MR, in that it is blocked by concurrent administration of the MR antagonist potassium canrenoate; and (vi) may or may not be a direct cardiac effect, inasmuch as data for in vivo effects on collagen formation by cardiac fibroblasts are conflicting.


In extending these initial findings, we have shown that cardiac fibrosis (i) is not reversed by correction of mineralocorticoid-induced hypokalemia; (ii) appears not to involve the plasma or tissue renin-angiotensin systems, as fibrosis is largely unaffected by concurrent administration of Losartan or Perindopril; (iii) is independent of cardiac hypertrophy, in that it is equally seen in right and left ventricles, and in rats rendered hypertensive without cardiac hypertrophy by the administration of 9 alpha-fluorocortisol; (iv) is independent of elevated blood pressure, in that it is found in normotensive animals infused peripherally with aldosterone and intracerebroventricularly with the mineralocorticoid receptor (<< MR >>) antagonist [[ RU28318 ]]; (v) is via classical MR, in that it is blocked by concurrent administration of the MR antagonist potassium canrenoate; and (vi) may or may not be a direct cardiac effect, inasmuch as data for in vivo effects on collagen formation by cardiac fibroblasts are conflicting.


In extending these initial findings, we have shown that cardiac fibrosis (i) is not reversed by correction of mineralocorticoid-induced hypokalemia; (ii) appears not to involve the plasma or tissue renin-angiotensin systems, as fibrosis is largely unaffected by concurrent administration of Losartan or Perindopril; (iii) is independent of cardiac hypertrophy, in that it is equally seen in right and left ventricles, and in rats rendered hypertensive without cardiac hypertrophy by the administration of 9 alpha-fluorocortisol; (iv) is independent of elevated blood pressure, in that it is found in normotensive animals infused peripherally with aldosterone and intracerebroventricularly with the mineralocorticoid receptor (MR) antagonist RU28318; (v) is via classical << MR >>, in that it is blocked by concurrent administration of the MR antagonist [[ potassium canrenoate ]]; and (vi) may or may not be a direct cardiac effect, inasmuch as data for in vivo effects on collagen formation by cardiac fibroblasts are conflicting.


In extending these initial findings, we have shown that cardiac fibrosis (i) is not reversed by correction of mineralocorticoid-induced hypokalemia; (ii) appears not to involve the plasma or tissue renin-angiotensin systems, as fibrosis is largely unaffected by concurrent administration of Losartan or Perindopril; (iii) is independent of cardiac hypertrophy, in that it is equally seen in right and left ventricles, and in rats rendered hypertensive without cardiac hypertrophy by the administration of 9 alpha-fluorocortisol; (iv) is independent of elevated blood pressure, in that it is found in normotensive animals infused peripherally with aldosterone and intracerebroventricularly with the mineralocorticoid receptor (MR) antagonist RU28318; (v) is via classical MR, in that it is blocked by concurrent administration of the << MR >> antagonist [[ potassium canrenoate ]]; and (vi) may or may not be a direct cardiac effect, inasmuch as data for in vivo effects on collagen formation by cardiac fibroblasts are conflicting.


<< Amezinium >> and debrisoquine are substrates of uptake1 and potent inhibitors of [[ monoamine oxidase ]] in perfused lungs of rats.


Amezinium and << debrisoquine >> are substrates of uptake1 and potent inhibitors of [[ monoamine oxidase ]] in perfused lungs of rats.


<< Amezinium >> and debrisoquine are substrates of [[ uptake1 ]] and potent inhibitors of monoamine oxidase in perfused lungs of rats.


Amezinium and << debrisoquine >> are substrates of [[ uptake1 ]] and potent inhibitors of monoamine oxidase in perfused lungs of rats.


Previous studies have resulted in the classification of << amezinium >> as a selective inhibitor of neuronal [[ monoamine oxidase ]] (MAO), because it is a much more potent MAO inhibitor in intact tissues, in which it is accumulated in noradrenergic neurones by uptake1, than in tissue homogenates.


Previous studies have resulted in the classification of << amezinium >> as a selective inhibitor of neuronal monoamine oxidase ([[ MAO ]]), because it is a much more potent MAO inhibitor in intact tissues, in which it is accumulated in noradrenergic neurones by uptake1, than in tissue homogenates.


Previous studies have resulted in the classification of << amezinium >> as a selective inhibitor of neuronal monoamine oxidase (MAO), because it is a much more potent [[ MAO ]] inhibitor in intact tissues, in which it is accumulated in noradrenergic neurones by uptake1, than in tissue homogenates.


In addition, another drug that is both a substrate of uptake1 and a << MAO >> inhibitor, [[ debrisoquine ]], was investigated in the study.


In addition, another drug that is both a substrate of << uptake1 >> and a MAO inhibitor, [[ debrisoquine ]], was investigated in the study.


When MAO-B was also inhibited, 10 nmol/l << amezinium >> caused 84% inhibition of the deamination of noradrenaline by [[ MAO-A ]] in the lungs.


The results when considered with previous reports in the literature show that << amezinium >> is about 1000 times more potent and debrisoquine is about 20 times more potent for [[ MAO ]] inhibition in rat lungs than in tissue homogenates, and the reason for their high potencies in the intact lungs is transport and accumulation of the drugs in the pulmonary endothelial cells by uptake1.


The results when considered with previous reports in the literature show that amezinium is about 1000 times more potent and << debrisoquine >> is about 20 times more potent for [[ MAO ]] inhibition in rat lungs than in tissue homogenates, and the reason for their high potencies in the intact lungs is transport and accumulation of the drugs in the pulmonary endothelial cells by uptake1.


The results when considered with previous reports in the literature show that << amezinium >> is about 1000 times more potent and debrisoquine is about 20 times more potent for MAO inhibition in rat lungs than in tissue homogenates, and the reason for their high potencies in the intact lungs is transport and accumulation of the drugs in the pulmonary endothelial cells by [[ uptake1 ]].


The results when considered with previous reports in the literature show that amezinium is about 1000 times more potent and << debrisoquine >> is about 20 times more potent for MAO inhibition in rat lungs than in tissue homogenates, and the reason for their high potencies in the intact lungs is transport and accumulation of the drugs in the pulmonary endothelial cells by [[ uptake1 ]].


<< Amezinium >> is much less potent as a [[ MAO ]] inhibitor in cells with the uptake2 transporter, such as the myocardial cells of the heart.


<< Amezinium >> is much less potent as a MAO inhibitor in cells with the [[ uptake2 transporter ]], such as the myocardial cells of the heart.


The results also confirmed previous reports that << amezinium >> is highly selective for [[ MAO-A ]].


We have investigated the effects of << CP-99,994 >> [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a [[ tachykinin NK1 receptor ]] antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.


We have investigated the effects of CP-99,994 << [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine] >>, a [[ tachykinin NK1 receptor ]] antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.


We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, << HOE 140 >> (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a [[ bradykinin B2 receptor ]] antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.


We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, HOE 140 << (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) >>, a [[ bradykinin B2 receptor ]] antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.


We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and << ketotifen >> (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a [[ histamine H1 receptor ]] antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.


We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and ketotifen << (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate) >>, a [[ histamine H1 receptor ]] antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.


Molecular determinants of << dofetilide >> block of [[ HERG ]] K+ channels.


Molecular determinants of << dofetilide >> block of HERG [[ K+ channels ]].


<< HERG >>/IKr channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as dofetilide, [[ E4031 ]], and MK-499, at submicromolar concentrations.


HERG/<< IKr >> channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as dofetilide, [[ E4031 ]], and MK-499, at submicromolar concentrations.


<< HERG >>/IKr channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as dofetilide, E4031, and [[ MK-499 ]], at submicromolar concentrations.


HERG/<< IKr >> channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as dofetilide, E4031, and [[ MK-499 ]], at submicromolar concentrations.


<< HERG >>/IKr channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic [[ methanesulfonanilide ]] drugs, such as dofetilide, E4031, and MK-499, at submicromolar concentrations.


HERG/<< IKr >> channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic [[ methanesulfonanilide ]] drugs, such as dofetilide, E4031, and MK-499, at submicromolar concentrations.


<< HERG >>/IKr channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as [[ dofetilide ]], E4031, and MK-499, at submicromolar concentrations.


HERG/<< IKr >> channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as [[ dofetilide ]], E4031, and MK-499, at submicromolar concentrations.


Treatment using a combination of testosterone and the << aromatase >> inhibitor [[ testolactone ]] may have significantly better effects on sexual function and also seizure frequency than testosterone alone.


A case of therapy-related acute myeloblastic leukemia with t(16;21)(q24;q22) after chemotherapy with << DNA-topoisomerase II >> inhibitors, [[ etoposide ]] and mitoxantrone, and the alkylating agent, cyclophosphamide.


A case of therapy-related acute myeloblastic leukemia with t(16;21)(q24;q22) after chemotherapy with << DNA-topoisomerase II >> inhibitors, etoposide and [[ mitoxantrone ]], and the alkylating agent, cyclophosphamide.


A 59-year-old female suffering from malignant lymphoma developed therapy-related acute myeloblastic leukemia (t-AML) after chemotherapy consisting of treatment with << DNA-topoisomerase II >> inhibitors, [[ etoposide ]] and mitoxantrone, and an alkylating agent, cyclophosphamide.


A 59-year-old female suffering from malignant lymphoma developed therapy-related acute myeloblastic leukemia (t-AML) after chemotherapy consisting of treatment with << DNA-topoisomerase II >> inhibitors, etoposide and [[ mitoxantrone ]], and an alkylating agent, cyclophosphamide.


<< Selegiline >> (deprenyl), a selective, irreversible inhibitor of [[ monoamine oxidase type B ]] (MAO-B) is widely used in the treatment of Parkinson's disease.


<< Selegiline >> (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B ([[ MAO-B ]]) is widely used in the treatment of Parkinson's disease.


Selegiline (<< deprenyl >>), a selective, irreversible inhibitor of [[ monoamine oxidase type B ]] (MAO-B) is widely used in the treatment of Parkinson's disease.


Selegiline (<< deprenyl >>), a selective, irreversible inhibitor of monoamine oxidase type B ([[ MAO-B ]]) is widely used in the treatment of Parkinson's disease.


Unlike the nonselective << MAO >> inhibitors, [[ selegiline ]] does not significantly potentiate tyramine-induced hypertension (the 'cheese effect') at the dosages (5 to 10 mg daily) used for the treatment of Parkinson's disease.


A low tyramine diet is recommended if << selegiline >> is used together with nonselective [[ MAO ]] inhibitors or the selective, reversible MAO-A inhibitor, moclobemide.


A low tyramine diet is recommended if selegiline is used together with nonselective MAO inhibitors or the selective, reversible << MAO-A >> inhibitor, [[ moclobemide ]].


<< Ibuprofen >> inhibits [[ cystic fibrosis transmembrane conductance regulator ]]-mediated Cl- secretion.


<< Ibuprofen >> (300 microM) reduced [[ CFTR ]] Cl- current by 60+/-16% and this was explained by a short-lived block (approximately 1.2 ms) which causes an apparent reduction in single channel amplitude from 1.07+/-0.04 pA to 0.59+/-0.04 pA (n = 3).


Similarly, << salicylic acid >> (3 mM) reduced [[ CFTR ]] Cl- current by 50+/-8% with an apparent reduction in single channel amplitude from 1.08+/-0.03 pA to 0.48+/-0.06 pA (n = 4).


Based on these results, we conclude that the NSAIDs << ibuprofen >> and salicylic acid inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of [[ CFTR ]] Cl- channels as well as basolateral membrane K+ channels.


Based on these results, we conclude that the NSAIDs << ibuprofen >> and salicylic acid inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of CFTR [[ Cl- channels ]] as well as basolateral membrane K+ channels.


Based on these results, we conclude that the NSAIDs << ibuprofen >> and salicylic acid inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of CFTR Cl- channels as well as basolateral membrane [[ K+ channels ]].


Based on these results, we conclude that the NSAIDs ibuprofen and << salicylic acid >> inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of [[ CFTR ]] Cl- channels as well as basolateral membrane K+ channels.


Based on these results, we conclude that the NSAIDs ibuprofen and << salicylic acid >> inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of CFTR [[ Cl- channels ]] as well as basolateral membrane K+ channels.


Based on these results, we conclude that the NSAIDs ibuprofen and << salicylic acid >> inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of CFTR Cl- channels as well as basolateral membrane [[ K+ channels ]].


Additional neuroendocrine experiments in a parallel group of rats revealed a dose-related increase in << plasma prolactin >> and ACTH levels after i.v. [[ mCPP ]], pointing to a general state of arousal in these mCPP-treated animals.


Additional neuroendocrine experiments in a parallel group of rats revealed a dose-related increase in plasma prolactin and << ACTH >> levels after i.v. [[ mCPP ]], pointing to a general state of arousal in these mCPP-treated animals.


These data indicate that mixed 5-HT1/5-HT2 receptor antagonists such as pizotifen and methysergide, and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective << 5-HT2A >>/5-HT2C antagonist [[ ritanserin ]].


These data indicate that mixed 5-HT1/5-HT2 receptor antagonists such as pizotifen and methysergide, and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/<< 5-HT2C >> antagonist [[ ritanserin ]].


These data indicate that mixed << 5-HT1 >>/5-HT2 receptor antagonists such as [[ pizotifen ]] and methysergide, and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/5-HT2C antagonist ritanserin.


These data indicate that mixed 5-HT1/<< 5-HT2 >> receptor antagonists such as [[ pizotifen ]] and methysergide, and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/5-HT2C antagonist ritanserin.


These data indicate that mixed << 5-HT1 >>/5-HT2 receptor antagonists such as pizotifen and [[ methysergide ]], and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/5-HT2C antagonist ritanserin.


These data indicate that mixed 5-HT1/<< 5-HT2 >> receptor antagonists such as pizotifen and [[ methysergide ]], and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/5-HT2C antagonist ritanserin.


The cardiovascular effects of three different << acetylcholinesterase >> inhibitors: [[ physostigmine ]], tacrine and rivastigmine injected by intravenous (i.v.) route were compared in freely moving Wistar rats.


The cardiovascular effects of three different << acetylcholinesterase >> inhibitors: physostigmine, [[ tacrine ]] and rivastigmine injected by intravenous (i.v.) route were compared in freely moving Wistar rats.


The cardiovascular effects of three different << acetylcholinesterase >> inhibitors: physostigmine, tacrine and [[ rivastigmine ]] injected by intravenous (i.v.) route were compared in freely moving Wistar rats.


<< Tacrine >> was chosen as a model to study the mechanisms underlying the cardiovascular effects of i.v. [[ cholinesterase ]] inhibitors.


The << alpha1-adrenoceptor >> antagonist [[ prazosin ]] or the vasopressin V1 receptor antagonist, [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8] vasopressin partially but significantly reduced tacrine pressor effect and mostly abolished it when administered concomitantly.


The alpha1-adrenoceptor antagonist prazosin or the << vasopressin V1 receptor >> antagonist, [[ [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8] vasopressin ]] partially but significantly reduced tacrine pressor effect and mostly abolished it when administered concomitantly.


The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective << muscarinic receptor >> antagonist [[ atropine ]] (ID50 = 1.45 microg), the muscarinic M1 receptor antagonist pirenzepine (ID50 = 4.33 microg), the muscarinic M2 receptor antagonist methoctramine (ID50 = 1.39 microg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50 = 31.19 microg).


The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50 = 1.45 microg), the << muscarinic M1 receptor >> antagonist [[ pirenzepine ]] (ID50 = 4.33 microg), the muscarinic M2 receptor antagonist methoctramine (ID50 = 1.39 microg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50 = 31.19 microg).


The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50 = 1.45 microg), the muscarinic M1 receptor antagonist pirenzepine (ID50 = 4.33 microg), the << muscarinic M2 receptor >> antagonist [[ methoctramine ]] (ID50 = 1.39 microg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50 = 31.19 microg).


The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50 = 1.45 microg), the muscarinic M1 receptor antagonist pirenzepine (ID50 = 4.33 microg), the muscarinic M2 receptor antagonist methoctramine (ID50 = 1.39 microg) and the << muscarinic M3 receptor >> antagonist [[ para-fluoro-hexahydro-sila-difenidol ]] (ID50 = 31.19 microg).


State-dependent << cocaine >> block of [[ sodium channel ]] isoforms, chimeras, and channels coexpressed with the beta1 subunit.


<< Cocaine >> block of [[ human cardiac (hH1) ]] and rat skeletal (mu1) muscle sodium channels was examined under whole-cell voltage clamp in transiently transfected HEK293t cells.


<< Cocaine >> block of human cardiac (hH1) and [[ rat skeletal (mu1) muscle sodium channels ]] was examined under whole-cell voltage clamp in transiently transfected HEK293t cells.


<< Cocaine >> block of [[ hH1 channels ]] was greater than block of mu1 channels at voltages between -120 mV and -90 mV, suggesting that greater steady-state inactivation of hH1 channels in this voltage range makes them more susceptible to cocaine block.


<< Cocaine >> block of hH1 channels was greater than block of [[ mu1 channels ]] at voltages between -120 mV and -90 mV, suggesting that greater steady-state inactivation of hH1 channels in this voltage range makes them more susceptible to cocaine block.


<< Cocaine >> block of hH1 channels was greater than block of mu1 channels at voltages between -120 mV and -90 mV, suggesting that greater steady-state inactivation of [[ hH1 channels ]] in this voltage range makes them more susceptible to cocaine block.


Cocaine block of hH1 channels was greater than block of mu1 channels at voltages between -120 mV and -90 mV, suggesting that greater steady-state inactivation of << hH1 channels >> in this voltage range makes them more susceptible to [[ cocaine ]] block.