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Article: α(1L)-Adrenoceptors in canine pulmonary artery

Titleα(1L)-Adrenoceptors in canine pulmonary artery
Authors
Issue Date1998
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1998, v. 32 n. 2, p. 308-316 How to Cite?
AbstractThe aim of this study was to characterize theα1-adrenoceptors of the canine pulmonary artery. Arterial rings from lower lung lobes were suspended for isometric-tension recording in the presence of cocaine (5 x 10-6 M), hydrocortisone (3 x 10-5 M), propranolol (5 x 10-6 M), and rauwolscine (10-7 M) to inhibit neuronal uptake, extraneuronal uptake, and β- and α2-adrenoceptors, respectively. Prazosin was more potent against contractions evoked by phenylephrine (pA2 of 9.7) compared with methoxamine (pA2 of 8.4). SZL49 (10-8 and 3 x 10-8 M), an irreversible α1- adrenergic antagonist, inhibited responses to phenylephrine but not methoxamine. With norepinephrine, low concentrations of prazosin (3 x 10- 10 M and 10-9 M) caused inhibition of the concentration-response curve; a higher concentration (3 x 10-9 M) failed to produced further inhibition, whereas increasing the concentration of the antagonist (to 10-8 and 3 x 10-8 M) caused further rightward shifts in the concentration-response curve. The Arunlakshana and Schild plot revealed two components corresponding to pA2 values of 9.8 and 8.4. After SZL49 (3 x 10-8 M), the Arunlakshana and Schild plot for the interaction between norepinephrine and prazosin was linear and generated a pA2 of 8.3. Contractions evoked by phenylephrine were inhibited by the α(1B)/α(1D)adrenoceptor antagonist, chloroethylclonidine (10-5 M), or by the α(1B)-antagonist, risperidone (pA2 value of 8.5), but were relatively resistant to inhibition by the selective α(1D)-antagonist, BMY7378 (-log K(B) of 6.1). The results suggest that two α1-adrenoceptor subtypes mediate contraction of the canine pulmonary artery. One subtype has high affinity for prazosin (α(1H), likely to be α(1B)), is activated by phenylephrine, and is inhibited by SZL49. The other subtype has lower affinity for prazosin (α(1L)), is stimulated by methoxamine, and is relatively resistant to SZL49. The physiologic agonist, norepinephrine, causes contraction by activating both subtypes.
Persistent Identifierhttp://hdl.handle.net/10722/171206
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorHales, MAen_US
dc.contributor.authorAleskowitch, TDen_US
dc.contributor.authorGaine, SPen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:42Z-
dc.date.available2012-10-30T06:12:42Z-
dc.date.issued1998en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1998, v. 32 n. 2, p. 308-316en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/171206-
dc.description.abstractThe aim of this study was to characterize theα1-adrenoceptors of the canine pulmonary artery. Arterial rings from lower lung lobes were suspended for isometric-tension recording in the presence of cocaine (5 x 10-6 M), hydrocortisone (3 x 10-5 M), propranolol (5 x 10-6 M), and rauwolscine (10-7 M) to inhibit neuronal uptake, extraneuronal uptake, and β- and α2-adrenoceptors, respectively. Prazosin was more potent against contractions evoked by phenylephrine (pA2 of 9.7) compared with methoxamine (pA2 of 8.4). SZL49 (10-8 and 3 x 10-8 M), an irreversible α1- adrenergic antagonist, inhibited responses to phenylephrine but not methoxamine. With norepinephrine, low concentrations of prazosin (3 x 10- 10 M and 10-9 M) caused inhibition of the concentration-response curve; a higher concentration (3 x 10-9 M) failed to produced further inhibition, whereas increasing the concentration of the antagonist (to 10-8 and 3 x 10-8 M) caused further rightward shifts in the concentration-response curve. The Arunlakshana and Schild plot revealed two components corresponding to pA2 values of 9.8 and 8.4. After SZL49 (3 x 10-8 M), the Arunlakshana and Schild plot for the interaction between norepinephrine and prazosin was linear and generated a pA2 of 8.3. Contractions evoked by phenylephrine were inhibited by the α(1B)/α(1D)adrenoceptor antagonist, chloroethylclonidine (10-5 M), or by the α(1B)-antagonist, risperidone (pA2 value of 8.5), but were relatively resistant to inhibition by the selective α(1D)-antagonist, BMY7378 (-log K(B) of 6.1). The results suggest that two α1-adrenoceptor subtypes mediate contraction of the canine pulmonary artery. One subtype has high affinity for prazosin (α(1H), likely to be α(1B)), is activated by phenylephrine, and is inhibited by SZL49. The other subtype has lower affinity for prazosin (α(1L)), is stimulated by methoxamine, and is relatively resistant to SZL49. The physiologic agonist, norepinephrine, causes contraction by activating both subtypes.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAdrenergic Alpha-1 Receptor Agonistsen_US
dc.subject.meshAdrenergic Alpha-1 Receptor Antagonistsen_US
dc.subject.meshAdrenergic Alpha-Agonists - Pharmacologyen_US
dc.subject.meshAdrenergic Alpha-Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Metabolism - Physiologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshPrazosin - Pharmacologyen_US
dc.subject.meshPulmonary Artery - Metabolismen_US
dc.subject.meshReceptors, Adrenergic, Alpha-1 - Metabolismen_US
dc.titleα(1L)-Adrenoceptors in canine pulmonary arteryen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00005344-199808000-00020en_US
dc.identifier.pmid9700995-
dc.identifier.scopuseid_2-s2.0-0031596405en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031596405&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume32en_US
dc.identifier.issue2en_US
dc.identifier.spage308en_US
dc.identifier.epage316en_US
dc.identifier.isiWOS:000075018700020-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridHales, MA=7004025965en_US
dc.identifier.scopusauthoridAleskowitch, TD=6507393851en_US
dc.identifier.scopusauthoridGaine, SP=35264010200en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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