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Article: α 2-Adrenoceptor antagonists evoke endothelium-dependent and - independent relaxations in the isolated rat aorta

Titleα 2-Adrenoceptor antagonists evoke endothelium-dependent and - independent relaxations in the isolated rat aorta
Authors
KeywordsΑ 2-Adrenoceptor Antagonists
Cyclic Gmp
Endothelium-Dependent And - Independent Relaxation
Nitric Oxide
Potassium Channels
Rat Aorta
Issue Date1999
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1999, v. 34 n. 1, p. 148-152 How to Cite?
AbstractThis study was designed to determine whether the α 2-adrenoceptor antagonists idazoxan, yohimbine, and rauwolscine cause endothelium-dependent and -independent responses in the rat aorta. Rings of rat aorta, with and without endothelium, were suspended for the measurement of isometric force in modified Krebs-Ringer bicarbonate solution (37°C; aerated with 95% O 2 and 5% CO 2). The α 2-adrenoceptor antagonists, in the concentration range of 10 -8-10 -6 M, relaxed phenylephrine-contracted rings with, but not those without endothelium, α 2-Adrenoceptor antagonists (3 x 10 -6 M for 1 min) increased the accumulation of cyclic guanosine monophosphate (cGMP) about twofold in the aortas with endothelium. The relaxation and the increased cGMP induced by α2-antagonists were attenuated by methylene blue (10 -6 M) and N(G)-nitro-L-arginine (L-NA, 3 x 10 -5 M), whereas propranolol (10 -6 M) did not affect the relaxation. In concentrations >10 -6 M, α 2-adrenoceptor antagonists relaxed the rat aorta without endothelium. The endothelium- independent relaxation by α 2-adrenoceptor antagonists was abolished by increased external K + and reduced significantly by tetraethylammonium (TEA, 10 -2 M, a Ca 2+-dependent K + channel blocker), but not inhibited by glibenclamide (10 -5 M, an ATP-sensitive K + channel blocker). In the rabbit aorta, only endothelium-independent relaxations were observed with α2- adrenoceptor antagonists in the concentration range of 10 -8-10 -5 M, and these relaxations were not antagonized by TEA. These results suggest that α 2-adrenoceptor antagonists relax the rat aorta through endothelium- dependent mechanism at lower concentrations and endothelium-independent mechanisms at higher concentrations. The endothelium-dependent relaxations are likely to be mediated by the endothelium-derived relaxing factor (EDRF)/NO pathway because they are associated with the accumulation of cGMP, whereas the endothelium-independent relaxations may be caused by the opening of potassium channels in the vascular smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/171228
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKim, NDen_US
dc.contributor.authorKang, KWen_US
dc.contributor.authorKang, SYen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:49Z-
dc.date.available2012-10-30T06:12:49Z-
dc.date.issued1999en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1999, v. 34 n. 1, p. 148-152en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/171228-
dc.description.abstractThis study was designed to determine whether the α 2-adrenoceptor antagonists idazoxan, yohimbine, and rauwolscine cause endothelium-dependent and -independent responses in the rat aorta. Rings of rat aorta, with and without endothelium, were suspended for the measurement of isometric force in modified Krebs-Ringer bicarbonate solution (37°C; aerated with 95% O 2 and 5% CO 2). The α 2-adrenoceptor antagonists, in the concentration range of 10 -8-10 -6 M, relaxed phenylephrine-contracted rings with, but not those without endothelium, α 2-Adrenoceptor antagonists (3 x 10 -6 M for 1 min) increased the accumulation of cyclic guanosine monophosphate (cGMP) about twofold in the aortas with endothelium. The relaxation and the increased cGMP induced by α2-antagonists were attenuated by methylene blue (10 -6 M) and N(G)-nitro-L-arginine (L-NA, 3 x 10 -5 M), whereas propranolol (10 -6 M) did not affect the relaxation. In concentrations >10 -6 M, α 2-adrenoceptor antagonists relaxed the rat aorta without endothelium. The endothelium- independent relaxation by α 2-adrenoceptor antagonists was abolished by increased external K + and reduced significantly by tetraethylammonium (TEA, 10 -2 M, a Ca 2+-dependent K + channel blocker), but not inhibited by glibenclamide (10 -5 M, an ATP-sensitive K + channel blocker). In the rabbit aorta, only endothelium-independent relaxations were observed with α2- adrenoceptor antagonists in the concentration range of 10 -8-10 -5 M, and these relaxations were not antagonized by TEA. These results suggest that α 2-adrenoceptor antagonists relax the rat aorta through endothelium- dependent mechanism at lower concentrations and endothelium-independent mechanisms at higher concentrations. The endothelium-dependent relaxations are likely to be mediated by the endothelium-derived relaxing factor (EDRF)/NO pathway because they are associated with the accumulation of cGMP, whereas the endothelium-independent relaxations may be caused by the opening of potassium channels in the vascular smooth muscle.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.subjectΑ 2-Adrenoceptor Antagonistsen_US
dc.subjectCyclic Gmpen_US
dc.subjectEndothelium-Dependent And - Independent Relaxationen_US
dc.subjectNitric Oxideen_US
dc.subjectPotassium Channelsen_US
dc.subjectRat Aortaen_US
dc.titleα 2-Adrenoceptor antagonists evoke endothelium-dependent and - independent relaxations in the isolated rat aortaen_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.doi10.1097/00005344-199907000-00023en_US
dc.identifier.pmid10413081-
dc.identifier.scopuseid_2-s2.0-0033160718en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033160718&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume34en_US
dc.identifier.issue1en_US
dc.identifier.spage148en_US
dc.identifier.epage152en_US
dc.identifier.isiWOS:000081087700023-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKim, ND=7409933438en_US
dc.identifier.scopusauthoridKang, KW=35233912600en_US
dc.identifier.scopusauthoridKang, SY=7405684253en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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