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Titolo:
ROLE OF L-ARGININE-DERIVED NITRIC-OXIDE IN CHOLINERGIC DILATION OF GASTRIC ARTERIOLES
Autore:
CHEN RYZ; ROSS G; CHYU KY; GUTH PH;
Indirizzi:
VET AFFAIRS MED CTR W LOS ANGELES,DEPT ANESTHESIOL W212,ANESTHESIOL MED & RES SERV LOS ANGELES CA 90073 UNIV CALIF LOS ANGELES,SCH MED LOS ANGELES CA 90073
Titolo Testata:
The American journal of physiology
fascicolo: 6, volume: 265, anno: 1993,
parte:, 2
pagine: 80002110 - 80002116
SICI:
0002-9513(1993)265:6<80002110:ROLNIC>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
MONOMETHYL-L-ARGININE; SKELETAL-MUSCLE; HYPERPOLARIZING FACTOR; ENDOTHELIAL-CELLS; RELAXING FACTOR; ACETYLCHOLINE; RAT; INVIVO; MICROCIRCULATION; VASODILATATION;
Keywords:
GASTRIC MICROCIRCULATION; ACETYLCHOLINE; ARGININE ANALOGS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
32
Recensione:
Indirizzi per estratti:
Citazione:
R.Y.Z. Chen et al., "ROLE OF L-ARGININE-DERIVED NITRIC-OXIDE IN CHOLINERGIC DILATION OF GASTRIC ARTERIOLES", The American journal of physiology, 265(6), 1993, pp. 80002110-80002116

Abstract

The role of L-arginine-derived nitric oxide (NO) in cholinergic vasodilation of resistance vessels was studied in the intact stomach of therat, utilizing an in vivo microscopy technique. Two L-arginine analogues, N(G)-monomethyl-L-arginine (L-NMMA) and nitro-L-arginine methyl ester (L-NAME), were used to block NO synthesis. Cholinergic dilation of gastric submucosal arterioles was induced by topical application of various concentrations of acetylcholine (ACh) (10(-7)-10(-4) M). Intravenous but not topical administration of L-NMMA and L-NAME caused an increase in arterial pressure. Intravenous or topical L-NAME reduces resting arteriolar diameter. These findings support the contention that NO formation modulates basal vascular tone and suggest that NO releasemay play a significant role in the regulation of the gastric circulation. L-Arginine analogues attenuated the arteriolar dilating effect ofACh but not adenosine or nitroglycerin. Substantial arteriolar responses to ACh remained after systemic or topical treatment with either L-NMMA or L-NAME. These results indicate that the L-arginine-NO pathway accounts only in part for ACh-induced vasodilation in gastric resistance vessels in vivo.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 13:34:44