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Titolo:
INHIBITION BY NICKEL OF ENDOTHELIN-1-INDUCED TENSION AND ASSOCIATED CA-45 MOVEMENTS IN RABBIT AORTA
Autore:
SHETTY SS; DELGRANDE D;
Indirizzi:
CIBA PHARMACEUT,LSB 2215,556 MORRIS AVE SUMMIT NJ 07901 CIBA GEIGY CORP,DEPT RES,DIV PHARMACEUT SUMMIT NJ 07901
Titolo Testata:
The Journal of pharmacology and experimental therapeutics
fascicolo: 3, volume: 271, anno: 1994,
pagine: 1223 - 1227
SICI:
0022-3565(1994)271:3<1223:IBNOET>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; CA-2+ CHANNEL; NOREPINEPHRINE; PEPTIDE; CELLS; POTASSIUM; MECHANISM; BINDING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
26
Recensione:
Indirizzi per estratti:
Citazione:
S.S. Shetty e D. Delgrande, "INHIBITION BY NICKEL OF ENDOTHELIN-1-INDUCED TENSION AND ASSOCIATED CA-45 MOVEMENTS IN RABBIT AORTA", The Journal of pharmacology and experimental therapeutics, 271(3), 1994, pp. 1223-1227

Abstract

Contractions induced by 10 nM endothelin-1 (ET) in the rabbit aortic media intimal layer were inhibited by prior exposure to 100 mu M Ni++ (33.1%) or to a Ca++-free buffer (80.2%) but were unaffected by pretreatment with 0.1 mu M nifedipine. Contractions elicited by phenylephrine (1 nM-100 mu M) or K+ (10-50 mM) were not inhibited by 100 mu M Ni+but those induced by ET in tissues submaximally precontracted with 20mM K+ were selectively antagonized by the divalent cation. The mechanism for the inhibitory action of Ni++ was ascertained by an examination of the effects of the cation on ET-induced alterations in the cellular distribution and mobilization of Ca++. Efflux of Ca-45 from the muscle into a solution without added Ca++ was not altered by ET. Total orcellular Ca-45 uptake (uptake after exposure to La+++ and low temperature), at either low- or high-affinity sites in resting muscles was also not affected by the peptide. However, low-affinity cellular Ca-45 retention in muscles depolarized with high K+ levels (160 mM) was significantly enhanced (45.1%) by ET. Ni++ did not alter Ca-45 retention incontrol and K+-treated muscles but it blocked the additional incremental Ca-45 uptake associated with ET (in the presence of high K+), Thus, Ni++ produced a selective blockade of an ET-activated Ca++ influx pathway, distinct from the dihydropyridine-sensitive L-type Ca++ channels, in rabbit aortic smooth muscle. This action by Ni++ apparently inhibits subsequent contractile responses of the muscle to ET.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 12:35:13