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Titolo:
ACUTE ENDOTHELIN-RECEPTOR INHIBITION DOES NOT ATTENUATE ACETYLCHOLINE-INDUCED CORONARY VASOCONSTRICTION IN EXPERIMENTAL HYPERCHOLESTEROLEMIA
Autore:
HASDAI D; BEST PJM; CANNAN CR; MATHEW V; SCHWARTZ RS; HOLMES DR; LERMAN A;
Indirizzi:
MAYO CLIN & MAYO FDN,DIV CARDIOVASC DIS,200 1ST ST SW ROCHESTER MN 55905 MAYO CLIN & MAYO FDN,DIV CARDIOVASC DIS ROCHESTER MN 55905 MAYO CLIN & MAYO FDN,DIV INTERNAL MED ROCHESTER MN 55905
Titolo Testata:
Arteriosclerosis, thrombosis, and vascular biology
fascicolo: 1, volume: 18, anno: 1998,
pagine: 108 - 113
SICI:
1079-5642(1998)18:1<108:AEIDNA>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONVERTING ENZYME-INHIBITION; ARTERY DISEASE; ET(B) RECEPTORS; MESSENGER-RNA; HEART-FAILURE; ATHEROSCLEROSIS; DYSFUNCTION; ANTAGONIST; IMMUNOREACTIVITY; HETEROGENEITY;
Keywords:
PIG; HYPERCHOLESTEROLEMIA; ACETYLCHOLINE; ENDOTHELIN; ENDOTHELIN RECEPTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
D. Hasdai et al., "ACUTE ENDOTHELIN-RECEPTOR INHIBITION DOES NOT ATTENUATE ACETYLCHOLINE-INDUCED CORONARY VASOCONSTRICTION IN EXPERIMENTAL HYPERCHOLESTEROLEMIA", Arteriosclerosis, thrombosis, and vascular biology, 18(1), 1998, pp. 108-113

Abstract

Endothelin (ET) may mediate the enhanced coronary vasoconstriction associated with hypercholesterolemia, We hypothesized that short-term inhibition of ET receptors attenuates the coronary epicardial vasoconstrictor response to acetylcholine in experimental hypercholesterolemia. ET-1 (group I, n=5; 5 ng.kg(-1).min(-1)) and acetylcholine (group III n=7; 10(-6) to 10(-4) mol/L) were given by intracoronary infusion in rigs, ET-1 and acetylcholine were also infused with the specific ETA-receptor blocker FR-139317 (5 mu g.kg(-1).min(-1); group II, n=6; group IV, n=6), Acetylcholine was also infused with the combined ET-receptorblocker, bosentan (0.5 mg/kg plus 1 mg.kg(-1).h(-1), group V, n=5). The ETB-receptor agonist sarafotoxin 6c (5 ng.kg(-1).min(-1); n=4) was also infused. The percentage change in coronary artery diameter (%Delta CAD) to the infusions was measured at baseline and after 10 weeks ofhigh-cholesterol diet ill all animals. Sarafotoxin 6c mildly reduced %Delta CAD at baseline and 10 weeks (-10+/-2% and -12+/-3%, respectively). FR-130317 did not attenuate the epicardial vasoconstrictor response to ET-1 at baseline (%Delta CAD -18+/-8% for group I versus -12+/-6% for group II; P=NS) but did at 10 weeks (%Delta CAD -77+/-14% for group I versus -14+/-6% for group II; P<.05). FR-139317 did not affect the response to acetylcholine at baseline (%Delta CAD 5+/-2% for group III versus 7+/-3% for group IV, P=NS) or at 10 weeks (%Delta CAD -23+/-12% for sour III versus -19+/-7% for soup IV; P=NS). Bosentan did notaffect the response to acetylcholine at baseline or 10 weeks. Short-term ET-receptor inhibition in experimental hypercholesterolemia attenuated the enhanced coronary epicardial vasoconstrictor effects of ET-1 but not acetylcholine-induced coronary epicardial vasoconstriction, suggesting that acetylcholine-induced coronary epicardial vasoconstriction may not be mediated by ET receptors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 20:40:47