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Titolo:
NITRIC-OXIDE ATTENUATES ENDOTHELIN-1-INDUCED VASOCONSTRICTION IN CANINE STOMACH
Autore:
WOOD JG; ZHANG Q; YAN ZY; CHEUNG LY;
Indirizzi:
UNIV KANSAS,MED CTR,DEPT SURG,3901 RAINBOW BLVD KANSAS CITY KS 66160 UNIV KANSAS,MED CTR,DEPT SURG KANSAS CITY KS 66160 UNIV KANSAS,MED CTR,DEPT PHYSIOL KANSAS CITY KS 66160
Titolo Testata:
American journal of physiology: Gastrointestinal and liver physiology
fascicolo: 1, volume: 34, anno: 1996,
pagine: 27 - 35
SICI:
0193-1857(1996)34:1<27:NAEVIC>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCARDIAL-ISCHEMIA; RELAXING FACTOR; GASTRIC MICROCIRCULATION; ENDOTHELIAL DYSFUNCTION; REPERFUSION; RAT; RELEASE; INHIBITION; SUPEROXIDE; MODULATION;
Keywords:
N-G-NITRO-L-ARGININE METHYL ESTER; NITRIC OXIDE DONOR; VASCULAR REACTIVITY; ISCHEMIA-REPERFUSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
J.G. Wood et al., "NITRIC-OXIDE ATTENUATES ENDOTHELIN-1-INDUCED VASOCONSTRICTION IN CANINE STOMACH", American journal of physiology: Gastrointestinal and liver physiology, 34(1), 1996, pp. 27-35

Abstract

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of ourpresent study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2)whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate 3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]butyl; a nitric oxide donor} attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses toET-1 under normal Conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

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Documento generato il 27/11/20 alle ore 12:25:27