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Article: A revisitation on the mechanism of action of KCl-induced vascular smooth muscle contraction: a key role of cation binding to the plasma membrane

TitleA revisitation on the mechanism of action of KCl-induced vascular smooth muscle contraction: a key role of cation binding to the plasma membrane
Authors
Issue Date1995
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
Biological Signals, 1995, v. 4 n. 3, p. 160-167 How to Cite?
AbstractAortic rings of Sprague-Dawley rats developed reproducible contractions in Ca-free, nominally Mg-free (2 microM), Na-free, K solution, but not in Ca-free, nominally Mg-free, K-free, Na solution. Further reduction of the residual Mg by 0.5 mM EDTA in the above solutions potentiated this K-induced contraction and allowed the development of a relatively small contraction in Na-rich medium, respectively. The amplitude of EDTA-enhanced, K-induced contraction was almost the same as the amplitude of contraction induced in K-rich ([K] = 142 mM), Ca-containing (2.5 mM) solution. Such K-induced contraction was completely inhibited by 38 mM Na and by 3 mM of Mg (and Ni or Cd). Nifedipine (1 microM) also inhibited aortic smooth muscle contraction produced in K-EDTA, Ca-free solution. Modulators of Ca in sarcoplasmic reticulum (ryanodine, caffeine and norephinephrine), Ca-ionophore (A-23187) and protein kinase C inhibitor (Calphostin C) had no effect on EDTA-enhanced, K-induced contraction. It was suggested that K-induced contraction in rat aorta is not dependent on the increase in cytosolic Ca following membrane depolarization, is not a result of the release of Ca from intracellular stores, and is not due to change of Ca sensitivity upon the activation of protein kinase C. We propose that the competition of K for Mg and Na at external binding sites on the plasma membranes of the smooth muscle cells is primarily responsible for the development of vascular contraction.
Persistent Identifierhttp://hdl.handle.net/10722/224680
ISSN

 

DC FieldValueLanguage
dc.contributor.authorKravtsov, GM-
dc.contributor.authorKwan, CY-
dc.date.accessioned2016-04-12T02:26:03Z-
dc.date.available2016-04-12T02:26:03Z-
dc.date.issued1995-
dc.identifier.citationBiological Signals, 1995, v. 4 n. 3, p. 160-167-
dc.identifier.issn1016-0922-
dc.identifier.urihttp://hdl.handle.net/10722/224680-
dc.description.abstractAortic rings of Sprague-Dawley rats developed reproducible contractions in Ca-free, nominally Mg-free (2 microM), Na-free, K solution, but not in Ca-free, nominally Mg-free, K-free, Na solution. Further reduction of the residual Mg by 0.5 mM EDTA in the above solutions potentiated this K-induced contraction and allowed the development of a relatively small contraction in Na-rich medium, respectively. The amplitude of EDTA-enhanced, K-induced contraction was almost the same as the amplitude of contraction induced in K-rich ([K] = 142 mM), Ca-containing (2.5 mM) solution. Such K-induced contraction was completely inhibited by 38 mM Na and by 3 mM of Mg (and Ni or Cd). Nifedipine (1 microM) also inhibited aortic smooth muscle contraction produced in K-EDTA, Ca-free solution. Modulators of Ca in sarcoplasmic reticulum (ryanodine, caffeine and norephinephrine), Ca-ionophore (A-23187) and protein kinase C inhibitor (Calphostin C) had no effect on EDTA-enhanced, K-induced contraction. It was suggested that K-induced contraction in rat aorta is not dependent on the increase in cytosolic Ca following membrane depolarization, is not a result of the release of Ca from intracellular stores, and is not due to change of Ca sensitivity upon the activation of protein kinase C. We propose that the competition of K for Mg and Na at external binding sites on the plasma membranes of the smooth muscle cells is primarily responsible for the development of vascular contraction.-
dc.languageeng-
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG-
dc.relation.ispartofBiological Signals-
dc.rightsBiological Signals. Copyright © S Karger AG.-
dc.subject.meshMuscle, smooth, vascular - drug effects - metabolism - physiology-
dc.subject.meshMuscle contraction - drug effects-
dc.subject.meshPotassium chloride - pharmacology-
dc.subject.meshProtein kinase c - antagonists & inhibitors - metabolism-
dc.subject.meshSarcoplasmic reticulum - metabolism-
dc.titleA revisitation on the mechanism of action of KCl-induced vascular smooth muscle contraction: a key role of cation binding to the plasma membrane-
dc.typeArticle-
dc.identifier.emailKwan, CY: cykwan@hkucc.hku.hk-
dc.identifier.pmid8750942-
dc.identifier.hkuros11245-
dc.identifier.volume4-
dc.identifier.issue3-
dc.identifier.spage160-
dc.identifier.epage167-
dc.publisher.placeSwitzerland-

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