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Titolo:
Intracellular alkalinization augments alpha(1)-adrenoceptor-mediated vasoconstriction by promotion of Ca2+ entry through the non-L-type Ca2+ channels
Autore:
Wakabayashi, I; Masui, H; Groschner, K;
Indirizzi:
Yamagata Univ, Sch Med, Dept Hyg & Prevent Med, Yamagata 9909585, Japan Yamagata Univ Yamagata Japan 9909585 revent Med, Yamagata 9909585, Japan Hyogo Med Univ, Dept Publ Hlth, Nishinomiya, Hyogo 6638501, Japan Hyogo Med Univ Nishinomiya Hyogo Japan 6638501 miya, Hyogo 6638501, Japan Karl Franzens Univ Graz, Dept Pharmacol & Toxicol, A-8010 Graz, Austria Karl Franzens Univ Graz Graz Austria A-8010 oxicol, A-8010 Graz, Austria
Titolo Testata:
EUROPEAN JOURNAL OF PHARMACOLOGY
fascicolo: 2, volume: 428, anno: 2001,
pagine: 251 - 259
SICI:
0014-2999(20011005)428:2<251:IAAAV>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; RAT AORTA; INDUCED CONTRACTIONS; NA+/H+ EXCHANGE; PORTAL-VEIN; PH; CELLS; MECHANISM; PATHWAYS; NH4CL;
Keywords:
cytosolic alkalosis; Na+/H+ exchange; ammonium chloride; Ca2+ channel, receptor-operated; smooth muscle, vascular; adrenoceptor agonist;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Wakabayashi, I Yamagata Univ, Sch Med, Dept Hyg & Prevent Med, Iida Nishi 2-2-2, Yamagata9909585, Japan Yamagata Univ Iida Nishi 2-2-2 Yamagata Japan 9909585 apan
Citazione:
I. Wakabayashi et al., "Intracellular alkalinization augments alpha(1)-adrenoceptor-mediated vasoconstriction by promotion of Ca2+ entry through the non-L-type Ca2+ channels", EUR J PHARM, 428(2), 2001, pp. 251-259

Abstract

Modulation by intracellular pH of the vasoconstriction induced by alpha -adrenoceptor agonists was investigated in isolated guinea pig aorta. NH4Cl (15 mM) increased intracellular pH of aortic smooth muscle cells by about 0.2 pH unit and significantly augmented KCl-induced contraction of aortic strips, whereas simultaneous administration of NH4Cl (15 mM) plus Na+ propionate (30 mM) failed to affect intracellular pH or contractility. NH4Cl (15 mM) potentiated contractions induced by alpha -adrenoceptor agonists, norepinephrine, phenylephrine and clonidine. Contraction induced by alpha (1)-selective adrenoceptor agonist, phenylephrine, but not that induced by norepinephrine or clonidine, was insensitive to inhibition by verapamil (1 muM). Phenylephrine-induced contraction was not affected by NH4Cl in Ca2+-free medium whereas extracellular Ca2+-induced contraction of phenylephrine-stimulated aorta was significantly augmented by NH4Cl. Consistently, Ca-45(2+) uptake into phenylephrine (1 muM)-stimulated aortic strips was increased by incubation with NH4Cl. The potentiating effects of NH4Cl on both phenylephrine-induced Ca2+ entry and contraction were antagonized by Na+ propionate. These results suggest that intracellular alkalinization facilitates alpha (1)-adrenoceptor-mediated vasoconstriction by facilitation of an agonist-induced Ca2+ entry pathway that is independent of L-type Ca2+ channels. (C) 2001 Elsevier Science B.V. All rights reserved.

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Documento generato il 23/01/20 alle ore 07:26:20