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Titolo:
INTERACTION OF ENDOGENOUS NITRIC-OXIDE AND CGRP IN SENSORY NEURON-INDUCED GASTRIC VASODILATION
Autore:
CHEN RYZ; GUTH PH;
Indirizzi:
W LOS ANGELES VET AFFAIRS MED CTR,DEPT ANESTHESIOL W212,ANESTHESIOL SERV LOS ANGELES CA 90073 W LOS ANGELES VET AFFAIRS MED CTR,MED SERV LOS ANGELES CA 90073 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV LOS ANGELES CA 90073 UNIV CALIF LOS ANGELES,SCH MED LOS ANGELES CA 90073
Titolo Testata:
American journal of physiology: Gastrointestinal and liver physiology
fascicolo: 5, volume: 31, anno: 1995,
pagine: 791 - 796
SICI:
0193-1857(1995)31:5<791:IOENAC>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENE-RELATED PEPTIDE; ACID BACK-DIFFUSION; MUCOSAL BLOOD-FLOW; INTRAGASTRIC CAPSAICIN; HYPEREMIC RESPONSE; MESENTERIC-ARTERY; NERVOUS-SYSTEM; BINDING-SITES; RAT STOMACH; CALCITONIN;
Keywords:
GASTRIC MICROCIRCULATION; CAPSAICIN-SENSITIVE SENSORY NERVES; CALCITONIN GENE-RELATED PEPTIDE; HUMAN CALCITONIN GENE-RELATED PEPTIDE-(8-37);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
31
Recensione:
Indirizzi per estratti:
Citazione:
R.Y.Z. Chen e P.H. Guth, "INTERACTION OF ENDOGENOUS NITRIC-OXIDE AND CGRP IN SENSORY NEURON-INDUCED GASTRIC VASODILATION", American journal of physiology: Gastrointestinal and liver physiology, 31(5), 1995, pp. 791-796

Abstract

Stimulation of capsaicin-sensitive sensory nerves induces gastric mucosal hyperemia, which is mediated in part by both calcitonin gene-related peptide (CGRP) and nitric oxide (NO). In the present study, we used in vivo microscopy in anesthetized rats to determine 1) whether these agents were released locally at the submucosal level and, if so, 2) whether CGRP dilates arterioles via release of endothelium-derived NO. Intragastric capsaicin (160 mu M) dilated submucosal arterioles from 25 +/- 3 to 67 +/- 8 mu m. The intragastric capsaicin-induced vasodilation was markedly reversed not only by intravenous administration of the NO synthesis inhibitor N-G-nitro-L-arginine methyl ester (L-NAME) but also by submucosal suffusion of either L-NAME or the CORP receptor antagonist human CGRP-(8-37). The latter findings indicate that both NO and CGRP are released locally at the submucosal level. Submucosal application of CGRP induced dose-dependent dilation of gastric submucosal arterioles, which was significantly attenuated by L-NAME. However, at the same degree of vasodilation (42 mu m), the dilation induced withsubmucosal CGRP was much less attenuated by NO synthesis inhibition (-28%) compared with that induced with intragastric capsaicin (-79%). This indicates that endothelium-derived NO released by CGRP was not theonly source of submucosal NO in the latter response. There must be another as yet undetermined source of submucosal NO, e.g., possibly nitroxidergic nerves.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 06:22:11