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Article: Role of gap junctions in the responses to EDHF in rat and guinea-pig small arteries

TitleRole of gap junctions in the responses to EDHF in rat and guinea-pig small arteries
Authors
Issue Date1999
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 1999, v. 128 n. 8, p. 1788-1794 How to Cite?
Abstract1. In guinea-pig internal carotid arteries with an intact endothelium, acetylcholine (10 μM) and levcromakalim (10 μM) each hyperpolarized the smooth muscle whereas a 5 mM elevation of extracellular K + was without effect. 2. Incubation of the carotid artery with the gap junction inhibitors carbenoxolone (100 μM) or gap 27 (500 μM) essentially abolished the hyperpolarization to acetylcholine but it was without effect on that to levcromakalim. Carbenoxolone had no effect on the acetylcholine-induced endothelial cell hyperpolarization but inhibited the smooth muscle hyperpolarization induced by the endothelial cell K + channel opener, 1-ethyl-2-benzimidazolinone (600 μM). 3. In rat hepatic and mesenteric arteries with endothelium, carbenoxolone (100 or 500 μM) depolarized the smooth muscle but did not modify hyperpolarizations induced by KCl or levcromakalim. In the mesenteric (but not the hepatic) artery, the acetylcholine-induced hyperpolarization was inhibited by carbenoxolone. 4. Phenylephrine (1 μM) depolarized the smooth muscle cells of intact hepatic and mesenteric arteries, an effect enhanced by carbenoxolone. Gap 27 did not have a depolarizing action. In the presence of phenylephrine, acetylcholine-induced hyperpolarization of both hepatic and mesenteric artery myocytes was partially inhibited by each of the gap junction inhibitors. 5 Collectively, the data suggest that gap junctions play some role in the EDHF (endothelium-derived hyperpolarizing factor) response in rat hepatic and mesenteric arteries. However, in the guinea-pig internal carotid artery, electrotonic propagation of endothelial cell hyperpolarizations via gap junctions may be the sole mechanism underlying the response previously attributed to EDHF.
Persistent Identifierhttp://hdl.handle.net/10722/171305
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorEdwards, Gen_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorGardener, MJen_US
dc.contributor.authorThollon, Cen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorWeston, AHen_US
dc.date.accessioned2012-10-30T06:13:17Z-
dc.date.available2012-10-30T06:13:17Z-
dc.date.issued1999en_US
dc.identifier.citationBritish Journal Of Pharmacology, 1999, v. 128 n. 8, p. 1788-1794en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171305-
dc.description.abstract1. In guinea-pig internal carotid arteries with an intact endothelium, acetylcholine (10 μM) and levcromakalim (10 μM) each hyperpolarized the smooth muscle whereas a 5 mM elevation of extracellular K + was without effect. 2. Incubation of the carotid artery with the gap junction inhibitors carbenoxolone (100 μM) or gap 27 (500 μM) essentially abolished the hyperpolarization to acetylcholine but it was without effect on that to levcromakalim. Carbenoxolone had no effect on the acetylcholine-induced endothelial cell hyperpolarization but inhibited the smooth muscle hyperpolarization induced by the endothelial cell K + channel opener, 1-ethyl-2-benzimidazolinone (600 μM). 3. In rat hepatic and mesenteric arteries with endothelium, carbenoxolone (100 or 500 μM) depolarized the smooth muscle but did not modify hyperpolarizations induced by KCl or levcromakalim. In the mesenteric (but not the hepatic) artery, the acetylcholine-induced hyperpolarization was inhibited by carbenoxolone. 4. Phenylephrine (1 μM) depolarized the smooth muscle cells of intact hepatic and mesenteric arteries, an effect enhanced by carbenoxolone. Gap 27 did not have a depolarizing action. In the presence of phenylephrine, acetylcholine-induced hyperpolarization of both hepatic and mesenteric artery myocytes was partially inhibited by each of the gap junction inhibitors. 5 Collectively, the data suggest that gap junctions play some role in the EDHF (endothelium-derived hyperpolarizing factor) response in rat hepatic and mesenteric arteries. However, in the guinea-pig internal carotid artery, electrotonic propagation of endothelial cell hyperpolarizations via gap junctions may be the sole mechanism underlying the response previously attributed to EDHF.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Ulcer Agents - Pharmacologyen_US
dc.subject.meshArteries - Drug Effects - Physiologyen_US
dc.subject.meshBiological Factors - Pharmacologyen_US
dc.subject.meshCarbenoxolone - Pharmacologyen_US
dc.subject.meshConnexins - Pharmacologyen_US
dc.subject.meshGap Junctions - Drug Effects - Physiologyen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effects - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshPotassium Chloride - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleRole of gap junctions in the responses to EDHF in rat and guinea-pig small arteriesen_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.doi10.1038/sj.bjp.0703009-
dc.identifier.pmid10588935-
dc.identifier.scopuseid_2-s2.0-0343593692en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0343593692&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume128en_US
dc.identifier.issue8en_US
dc.identifier.spage1788en_US
dc.identifier.epage1794en_US
dc.identifier.isiWOS:000084360300020-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridEdwards, G=7402317535en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridGardener, MJ=6603795865en_US
dc.identifier.scopusauthoridThollon, C=6602540205en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridWeston, AH=7102913361en_US

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