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Titolo:
ENDOTHELIN-1 DOES NOT MEDIATE THE ENDOTHELIUM-DEPENDENT HYPOXIC CONTRACTIONS OF SMALL PULMONARY-ARTERIES IN RATS
Autore:
LAZOR R; FEIHL F; WAEBER B; KUCERA P; PERRET C;
Indirizzi:
UNIV LAUSANNE HOSP,INST PATHOPHYSIOL LAUSANNE SWITZERLAND UNIV LAUSANNE,INST PHYSIOL CH-1015 LAUSANNE SWITZERLAND UNIV LAUSANNE HOSP,DIV HYPERTENS LAUSANNE SWITZERLAND
Titolo Testata:
Chest
fascicolo: 1, volume: 110, anno: 1996,
pagine: 189 - 197
SICI:
0012-3692(1996)110:1<189:EDNMTE>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESENTERIC-ARTERIES; RESISTANCE VESSELS; CGMP MECHANISMS; SMOOTH-MUSCLE; VASOCONSTRICTION; RESPONSES; RELAXATION; CELLS;
Keywords:
BOSENTAN; ENDOTHELIN RECEPTOR ANTAGONISTS; ENDOTHELIUM-DERIVED CONTRACTING FACTOR; HYPOXIC PULMONARY VASOCONSTRICTION; ISOLATED SMALL PULMONARY ARTERY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
R. Lazor et al., "ENDOTHELIN-1 DOES NOT MEDIATE THE ENDOTHELIUM-DEPENDENT HYPOXIC CONTRACTIONS OF SMALL PULMONARY-ARTERIES IN RATS", Chest, 110(1), 1996, pp. 189-197

Abstract

Various pulmonary artery preparations in vitro demonstrate sustained endothelium-dependent contractions upon hypoxia. To determine whether endothelin-l could mediate this phenomenon, we examined the effect of bosentan, a new antagonist of both the ETA and ETB subtypes of the endothelin receptor. Small (300 mu m) pulmonary arteries from rats were mounted on a myograph, precontracted with prostaglandin F-2 alpha, and exposed to hypoxia (PO2, 10 to 15 mm Hg, measured on-line) for 45 min. Endothelium-intact control rings exhibited a biphasic response, with a transient initial vasoconstriction (phase 1) followed by a second slowly developing sustained contraction (phase 2). Expressed in percent of tile maximal response to 80 mmol/L KCl, the amplitudes of phase 1 (peak tension) and 2 (tension after 45 min of hypoxia) averaged 37+/-12% and 17+/-14%, respectively (n=11). In endothelium-denuded rings, phase 1 persisted while the amplitude of phase 2 was reduced to 2+/-12% (p<0.05, n=8), showing the endothelium dependence of this contraction. Neither phase was significantly decreased in rings treated with 10(-5)mmol/L bosentan (38+/-15% and 17+12%, respectively, n=6). The PO2 threshold for onset of hypoxic contraction was not significantly different among these three groups and averaged 32+/-24 mm Hg. In a separate experiment, we assessed the inhibitory effect of 10(-5) mol/L bosentan on the response to 10(-8) mol/L endothelin-1. Rings treated for 45 minwith 10(-8) mol/L endothelin-1 alone exhibited a maximal contraction of 75+/-27% (n=6). This was reduced to 4+/-17% (p<0.01, n=6) in rings treated with both 10(-8) mol/L endothelin-1 and 10(-5) mol/L bosentan. We conclude that complete blockade of all endothelin receptor subtypes has no effect on either endothelium-dependent or -independent hypoxic contractions in this preparation. This suggests that endothelial factors other than endothelin-1 mediate the acute hypoxic contractions ofsmall pulmonary arteries in the rat.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/08/20 alle ore 02:12:23