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Titolo:
CONTRACTION TO ENDOTHELIN-1 IN PULMONARY-ARTERIES FROM ENDOTOXIN-TREATED RATS IS MODULATED BY ENDOTHELIUM
Autore:
CURZEN NP; GRIFFITHS MJD; EVANS TW;
Indirizzi:
ROYAL BROMPTON HOSP,SYDNEY ST LONDON SW3 6NP ENGLAND NATL HEART & LUNG INST,CRIT CARE UNIT LONDON SW3 6LY ENGLAND
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 6, volume: 37, anno: 1995,
pagine: 2260 - 2266
SICI:
0363-6135(1995)37:6<2260:CTEIPF>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE; RECEPTOR; RELEASE; AORTA; PROSTACYCLIN; PEPTIDES; CLONING; SUBTYPE; FAILURE; CELLS;
Keywords:
SEPSIS; PULMONARY VASCULATURE; ENDOTHELINS; THROMBOXANE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
N.P. Curzen et al., "CONTRACTION TO ENDOTHELIN-1 IN PULMONARY-ARTERIES FROM ENDOTOXIN-TREATED RATS IS MODULATED BY ENDOTHELIUM", American journal of physiology. Heart and circulatory physiology, 37(6), 1995, pp. 2260-2266

Abstract

Sepsis is characterized by hyporesponsiveness of vascular smooth muscle to presser agents. Levels of the potent vasoconstrictor, endothelin-1 (ET-1), are elevated in animal models of sepsis and in patients. This study assesses the contractile response of pulmonary artery from endotoxin-pretreated rats to ET-1 to determine whether this contraction is modified by the endothelium. Both intact and denuded rings from endotoxin-pretreated rats exhibited hyporesponsiveness to ET-1, but the endothelium was found to be essential for maximal ET-1-induced contraction. Upon pretreatment of vessels with the cyclooxygenase inhibitor, indomethacin (10(-5) M), the novel ET(B)-receptor antagonist, BQ-788 (10(-8) and 10(-6) M), and the thromboxane At-receptor antagonist, ICI-192605 (10(-5) M), each of these agents caused a reduction in the ET-1-induced contraction of endotoxin-pretreated rat pulmonary artery only in the presence of the endothelium but had no effect in endothelium-denuded vessels or in sham-treated groups. These findings demonstrate that ET-1-induced contraction in pulmonary arteries from septic rats is partially dependent upon an endothelially derived cyclooxygenase product, the release of which appears to involve ET(B)-receptor stimulation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 19:54:09