File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Activation of protein kinase C as a modulator of potentiated UK-14304-induced contraction in dog mesentene artery and vein

TitleActivation of protein kinase C as a modulator of potentiated UK-14304-induced contraction in dog mesentene artery and vein
Authors
Issue Date1995
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal of Cardiovascular Pharmacology, 1995, v. 26 n. 6, p. 923-931 How to Cite?
AbstractWe assessed the role of protein kinase C (PKC) in the mechanism responsible for the potentiation of UK-14304-induced contractions produced when isolated dog mesenteric vascular rings were pretreated with threshold concentrations of 12-O-tetradecanoyl-phorbol-13-acetate (TPA), KCl, or endothelin-1 (ET-1). In dog mesenteric artery. UK-14304 produced a biphasic concentration-response curve in the presence of TPA, KCl, or ET-1, with the curve portion at lower concentrations being alpha 2-adrenoceptor dependent and the portion at higher concentrations being alpha 1-adrenoceptor dependent. Calphostin C (10(-6)M), a PKC inhibitor, abolished amplified UK-14304-induced contraction in the TPA-pretreated tissues. In the KCl- and ET-1-pretreated tissues. 10(-6)M calphostin C antagonized amplified UK-14304-induced contractions by approximately 20% in both parts of the concentration-response curve. In contrast, in dog mesenteric vein, amplified UK-14304-induced contractions by TPA, KCl, and ET-1 were entirely dependent on alpha 2-adrenoceptors. Calphostin C (10(-6)M), which in control experiments had no effect on KCl-induced contraction and antagonized responses to TPA by 60.1%, inhibited UK-14304-induced contraction by 18.3%. Amplified UK-14304-induced contraction was antagonized by 10(-6)M calphostin C by 21.8% in KCl-precontracted tissues, 58.1% in ET-1-precontracted tissues, and 66.3% in TPA-precontracted tissues. In the ET-1- and TPA-pretreated dog mesenteric veins, 10(-6)M calphostin C decreased maximal tensions of enhanced UK-14304-induced contractions to the same level as the UK-14304-induced maximal tension inhibited by 10(-6)M calphostin C in untreated dog mesenteric vein. Therefore, TPA can be a precontracting agent that amplifies UK-14304-induced contractions through PKC activation in both dog mesenteric artery and vein. PKC predominantly mediates the contraction amplification mechanisms after exposure to ET-1 in dog mesenteric vein and does not play a major role in the amplification of UK-14304-induced contraction by KCl in both dog mesenteric artery and vein. These data show that a common mechanism need not underlie amplification of adrenergic responses in mesenteric artery and vein.
Persistent Identifierhttp://hdl.handle.net/10722/225143
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962

 

DC FieldValueLanguage
dc.contributor.authorShimamoto, H-
dc.contributor.authorShimamoto, Y-
dc.contributor.authorKwan, DCY-
dc.contributor.authorDaniel, EE-
dc.date.accessioned2016-04-22T07:07:18Z-
dc.date.available2016-04-22T07:07:18Z-
dc.date.issued1995-
dc.identifier.citationJournal of Cardiovascular Pharmacology, 1995, v. 26 n. 6, p. 923-931-
dc.identifier.issn0160-2446-
dc.identifier.urihttp://hdl.handle.net/10722/225143-
dc.description.abstractWe assessed the role of protein kinase C (PKC) in the mechanism responsible for the potentiation of UK-14304-induced contractions produced when isolated dog mesenteric vascular rings were pretreated with threshold concentrations of 12-O-tetradecanoyl-phorbol-13-acetate (TPA), KCl, or endothelin-1 (ET-1). In dog mesenteric artery. UK-14304 produced a biphasic concentration-response curve in the presence of TPA, KCl, or ET-1, with the curve portion at lower concentrations being alpha 2-adrenoceptor dependent and the portion at higher concentrations being alpha 1-adrenoceptor dependent. Calphostin C (10(-6)M), a PKC inhibitor, abolished amplified UK-14304-induced contraction in the TPA-pretreated tissues. In the KCl- and ET-1-pretreated tissues. 10(-6)M calphostin C antagonized amplified UK-14304-induced contractions by approximately 20% in both parts of the concentration-response curve. In contrast, in dog mesenteric vein, amplified UK-14304-induced contractions by TPA, KCl, and ET-1 were entirely dependent on alpha 2-adrenoceptors. Calphostin C (10(-6)M), which in control experiments had no effect on KCl-induced contraction and antagonized responses to TPA by 60.1%, inhibited UK-14304-induced contraction by 18.3%. Amplified UK-14304-induced contraction was antagonized by 10(-6)M calphostin C by 21.8% in KCl-precontracted tissues, 58.1% in ET-1-precontracted tissues, and 66.3% in TPA-precontracted tissues. In the ET-1- and TPA-pretreated dog mesenteric veins, 10(-6)M calphostin C decreased maximal tensions of enhanced UK-14304-induced contractions to the same level as the UK-14304-induced maximal tension inhibited by 10(-6)M calphostin C in untreated dog mesenteric vein. Therefore, TPA can be a precontracting agent that amplifies UK-14304-induced contractions through PKC activation in both dog mesenteric artery and vein. PKC predominantly mediates the contraction amplification mechanisms after exposure to ET-1 in dog mesenteric vein and does not play a major role in the amplification of UK-14304-induced contraction by KCl in both dog mesenteric artery and vein. These data show that a common mechanism need not underlie amplification of adrenergic responses in mesenteric artery and vein.-
dc.languageeng-
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/-
dc.relation.ispartofJournal of Cardiovascular Pharmacology-
dc.rightsThis is a non-final version of an article published in final form in (provide complete journal citation)-
dc.subject.meshAdrenergic alpha-Agonists - pharmacology-
dc.subject.meshMesenteric Arteries - drug effects - physiology-
dc.subject.meshProtein Kinase C - physiology-
dc.subject.meshQuinoxalines - pharmacology-
dc.subject.meshVasoconstriction - drug effects-
dc.titleActivation of protein kinase C as a modulator of potentiated UK-14304-induced contraction in dog mesentene artery and vein-
dc.typeArticle-
dc.identifier.emailKwan, DCY: cykwan@hkucc.hku.hk-
dc.identifier.doi10.1097/00005344-199512000-00011-
dc.identifier.pmid8606529-
dc.identifier.hkuros11234-
dc.identifier.volume26-
dc.identifier.issue6-
dc.identifier.spage923-
dc.identifier.epage931-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats