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Titolo:
The influence of chloroethylclonidine-induced contraction in isolated arteries of Wistar Kyoto rats: alpha(1D)- and alpha(1A)-adrenoceptors, protein kinase C, and calcium influx
Autore:
Ibarra, M; Lopez-Guerrero, JJ; Villalobos-Molina, R;
Indirizzi:
Inst Politecn Nacl, CINVESTAV, Dept Farmacobiol, Mexico City 14000, DF, Mexico Inst Politecn Nacl Mexico City DF Mexico 14000 ico City 14000, DF, Mexico
Titolo Testata:
ARCHIVES OF MEDICAL RESEARCH
fascicolo: 4, volume: 32, anno: 2001,
pagine: 258 - 262
SICI:
0188-4409(200107/08)32:4<258:TIOCCI>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPONTANEOUSLY HYPERTENSIVE RATS; VASCULAR SMOOTH-MUSCLE; ADRENOCEPTOR-MEDIATED ACTIONS; MESENTERIC SMALL ARTERIES; ALPHA(1)-ADRENOCEPTOR SUBTYPES; BLOOD-VESSELS; AORTA; ALPHA-1-ADRENOCEPTORS; CHLORETHYLCLONIDINE; AGONIST;
Keywords:
calphostin C; nitrendipine; aorta; tail artery; chloroethylclonidine; Wistar Kyoto rats; alpha(1A)-adrenoceptors; alpha(1D)-adrenoceptors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Ibarra, M Inst Politecn Nacl, CINVESTAV, Dept Farmacobiol, Apdo Postal 22026, MexicoCity 14000, DF, Mexico Inst Politecn Nacl Apdo Postal 22026 Mexico City DF Mexico 14000
Citazione:
M. Ibarra et al., "The influence of chloroethylclonidine-induced contraction in isolated arteries of Wistar Kyoto rats: alpha(1D)- and alpha(1A)-adrenoceptors, protein kinase C, and calcium influx", ARCH MED R, 32(4), 2001, pp. 258-262

Abstract

Background. It has recently been reported that chloroethylclonidine (CEC) elicited contraction in tail arteries (alpha (1A)-adrenoceptors) and aorta (alpha (1D)-adrenoceptors) from normotensive and spontaneously hypertensiverats (SHR). This study investigated the relationship between CEC-induced contraction and the role of protein kinase C (PKC) and extracellular Cati influx in tail arteries and aorta from Wistar Kyoto rats (WKY). Methods. Time-course of CEC-induced contraction in endothelium-denuded arteries from Wistar, WKY, and SHR rats was evaluated. In WKY arteries, calphostin C (1 x 10(-6) M) and nitrendipine (1 x 10(-6) M) were used to determine the role of PKC and extracellular Ca++ in the contractile response to CECI respectively. Results. Chloroethylclonidine (1 x 10(-4) M) elicited contraction in tail arteries and aorta from normotensive and hypertensive rats. Maximal response to CEC was similar in tail arteries among strains (approximate to 30% of norepinephrine effect), while in aorta CEC elicited a higher contraction inWKY and SHR than in Wistar (59, 86, and 18% of norepinephrine effect, respectively). CEC-elicited maximal contractile responses were reached in 5 minin tail arteries and in 30-45 min in aorta irrespective of the rat strain,suggesting that different intracellular signaling pathways are involved inthe contractile response to CEC in these arteries. In WKY tail arteries, calphostin C and nitrendipine blocked CEC-induced contraction while in aortanitrendipine, but not calphostin C, inhibited CEC action. Conclusions. This study confirms marked strain-dependent differences in rat aorta responsiveness to CEC and suggests a central role for PKC in response to CEC in tail arteries and for extracellular Ca++ influx in aorta. (C) 2001 IMSS. Published by Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 10:03:14