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Titolo:
VASCULAR EFFECTS AND MECHANISM OF ACTION OF ENDOTHELIN-1 IN ISOLATED-PERFUSED PIG SKIN
Autore:
PANG CY; YANG RZ; NELIGAN P; XU N; CHIU C; ZHONG AG; FORREST CR;
Indirizzi:
HOSP SICK CHILDREN,RES INST,555 UNIV AVE TORONTO ON M5G 1X8 CANADA UNIV TORONTO,DEPT SURG TORONTO ON M5G 1X8 CANADA UNIV TORONTO,DEPT PHYSIOL TORONTO ON M5G 1X8 CANADA
Titolo Testata:
Journal of applied physiology
fascicolo: 6, volume: 79, anno: 1995,
pagine: 2106 - 2113
SICI:
8750-7587(1995)79:6<2106:VEAMOA>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE; BLOOD-FLOW; BIG ENDOTHELIN-1; MESSENGER-RNA; BINDING-SITES; PORCINE SKIN; CELLS; FLAP; MICROVASCULATURE; EXPRESSION;
Keywords:
L-TYPE CALCIUM CHANNELS; PHOSPHOLIPASE C; PROTEIN KINASE C; CUTANEOUS VASOCONSTRICTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
C.Y. Pang et al., "VASCULAR EFFECTS AND MECHANISM OF ACTION OF ENDOTHELIN-1 IN ISOLATED-PERFUSED PIG SKIN", Journal of applied physiology, 79(6), 1995, pp. 2106-2113

Abstract

We investigated the vascular effects and mechanism of action of endothelin-1 (ET-1) in the skin by intra-arterial infusion of ET-1 and its precursor Big ET-1 via a direct cutaneous artery in isolated perfused pig skin flaps (6 x 16 cm). The vascular contractivity was studied by monitoring the perfusion pressure in the skin flap. There was evidenceto indicate local conversion of Big ET-1 to ET-1 in the pig skin. It was also observed that ET-1 was a potent long-lasting vasoconstrictor with a potency of similar to 10- and 300-fold higher than those of BigET-1 and norepinephrine, respectively. The vasoconstrictor action of ET-1 was blocked (P < 0.01) by a selective ET(A)-receptor antagonist (BQ-123 or BQ-610; 10(-7) M) and enhanced (P < 0.05) by a nitric oxide synthase inhibitor (N-G-monomethyl-L-arginine or N-omega-nitro-L-arginine methyl ester; 10(-5) M). ET-1-induced increase in perfusion pressure was attenuated (P < 0.05) by an L-type Ca2+-channel antagonist (nitrendipine, verapamil, or nifedipine; 10(-5) M) and by removal of Ca2+ from the perfusate. ET-1-induced increase in perfusion pressure was also attenuated (P < 0.05) by a phospholipase C inhibitor (neomycin; 10(-2) M), a protein kinase C (PKC) inhibitor (chelerythrine or H-7; 10(-5) M), and an intracellular Ca2+ chelator 2-bis(2-aminophenoxy)]ethane-N,N,N',N'-tetraacetic acid (BAPTA); 10(-5) M]. Furthermore, it was observed that the concentration-dependent (5 x 10(-8) to 10(-5) M) increase in perfusion pressure induced by phorbol 12,13-dibutyrate, a PKC activator, was not affected by verapamil (10(-5) M) or removal of Ca2+ from the perfusate. Taken together, these observations suggest that the vasoconstrictor mechanism of ET-1 in the pig skin involved activation of ET(A) receptors, L-type Ca2+ channels, phospholipase C, and PKC and that the vasoconstrictor effect caused by activation of PKC was independent of L-type Ca2+ channels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 07:26:58