File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Role of endothelial cell hyperpolarization in EDHF-mediated responses in the guinea-pig carotid artery

TitleRole of endothelial cell hyperpolarization in EDHF-mediated responses in the guinea-pig carotid artery
Authors
Issue Date2000
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, 2000, v. 129 n. 6, p. 1103-1112 How to Cite?
Abstract1. Experiments were performed to identify the potassium channels involved in the acetylcholine-induced endothelium-dependent hyperpolarization of the guinea-pig internal carotid artery. Smooth muscle and endothelial cell membrane potentials were recorded in isolated arteries with intracellular microelectrodes. Potassium currents were recorded in freshly-dissociated smooth muscle cells using patch clamp techniques. 2. In single myocytes, iberiotoxin (0.1 μM)-, charybdotoxin (0.1 μM)-, apamin (0.5 μM)- and 4-aminopyridine (5 mM)-sensitive potassium currents were identified indicating the presence of large- and small-conductance calcium-sensitive potassium channels (BK(Ca) and SK(Ca)) as well as voltage-dependent potassium channels (K(v)). Charybdotoxin and iberiotoxin inhibited the same population of BK(Ca) but a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected. 4-aminopyridine (0.1-25 mM) induced a concentration-dependent inhibition of K(v) without affecting the iberiotoxin- or the apamin-sensitive currents. 3. In isolated arteries, both the endothelium-dependent hyperpolarization of smooth muscle and the hyperpolarization of endothelial cells induced by acetylcholine or by substance P were inhibited by 5 mM 4-aminopyridine. 4. These results indicate that in the vascular smooth muscle cells of the guinea-pig carotid artery, a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected, comforting the hypothesis that the combination of these two toxins should act on the endothelial cells. Furthermore, the inhibition by 4-aminopyridine of both smooth muscle and endothelial hyperpolarizations, suggests that in order to observe an endothelium-dependent hyperpolarization of the vascular smooth muscle cells, the activation of endothelial potassium channels is likely to be required.
Persistent Identifierhttp://hdl.handle.net/10722/171245
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorQuignard, JFen_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorEdwards, Gen_US
dc.contributor.authorDuhault, Jen_US
dc.contributor.authorWeston, AHen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:55Z-
dc.date.available2012-10-30T06:12:55Z-
dc.date.issued2000en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2000, v. 129 n. 6, p. 1103-1112en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171245-
dc.description.abstract1. Experiments were performed to identify the potassium channels involved in the acetylcholine-induced endothelium-dependent hyperpolarization of the guinea-pig internal carotid artery. Smooth muscle and endothelial cell membrane potentials were recorded in isolated arteries with intracellular microelectrodes. Potassium currents were recorded in freshly-dissociated smooth muscle cells using patch clamp techniques. 2. In single myocytes, iberiotoxin (0.1 μM)-, charybdotoxin (0.1 μM)-, apamin (0.5 μM)- and 4-aminopyridine (5 mM)-sensitive potassium currents were identified indicating the presence of large- and small-conductance calcium-sensitive potassium channels (BK(Ca) and SK(Ca)) as well as voltage-dependent potassium channels (K(v)). Charybdotoxin and iberiotoxin inhibited the same population of BK(Ca) but a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected. 4-aminopyridine (0.1-25 mM) induced a concentration-dependent inhibition of K(v) without affecting the iberiotoxin- or the apamin-sensitive currents. 3. In isolated arteries, both the endothelium-dependent hyperpolarization of smooth muscle and the hyperpolarization of endothelial cells induced by acetylcholine or by substance P were inhibited by 5 mM 4-aminopyridine. 4. These results indicate that in the vascular smooth muscle cells of the guinea-pig carotid artery, a conductance specifically sensitive to the combination of charybdotoxin plus apamin could not be detected, comforting the hypothesis that the combination of these two toxins should act on the endothelial cells. Furthermore, the inhibition by 4-aminopyridine of both smooth muscle and endothelial hyperpolarizations, suggests that in order to observe an endothelium-dependent hyperpolarization of the vascular smooth muscle cells, the activation of endothelial potassium channels is likely to be required.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.mesh4-Aminopyridine - Pharmacologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCarotid Arteries - Drug Effectsen_US
dc.subject.meshCell Membrane - Drug Effects - Physiologyen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshEndothelium, Vascular - Cytology - Drug Effects - Physiologyen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Physiologyen_US
dc.subject.meshMicroelectrodesen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshPotassium Channel Blockersen_US
dc.subject.meshPotassium Channels - Drug Effectsen_US
dc.subject.meshSubstance P - Pharmacologyen_US
dc.titleRole of endothelial cell hyperpolarization in EDHF-mediated responses in the guinea-pig carotid 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.doi10.1038/sj.bjp.0703175-
dc.identifier.pmid10725258-
dc.identifier.scopuseid_2-s2.0-0034100629en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034100629&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume129en_US
dc.identifier.issue6en_US
dc.identifier.spage1103en_US
dc.identifier.epage1112en_US
dc.identifier.isiWOS:000085876000008-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridQuignard, JF=13606215800en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridEdwards, G=7402317535en_US
dc.identifier.scopusauthoridDuhault, J=7005108808en_US
dc.identifier.scopusauthoridWeston, AH=7102913361en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats