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Titolo:
Arterial relaxation mediated by endothelium-derived hyperpolarizing factorin hypertension induced by chronic inhibition of nitric oxide synthesis
Autore:
Kimura, K; Tsuda, K; Sasajima, H; Shiotani, M; Baba, A; Hano, T; Nishio, I;
Indirizzi:
Wakayama Med Coll, Dept Med, Div Cardiol, Wakayama 6408156, Japan WakayamaMed Coll Wakayama Japan 6408156 ardiol, Wakayama 6408156, Japan
Titolo Testata:
CLINICAL AND EXPERIMENTAL HYPERTENSION
fascicolo: 7, volume: 21, anno: 1999,
pagine: 1203 - 1221
SICI:
1064-1963(199910)21:7<1203:ARMBEH>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE RELAXATION; K+-CHANNELS; DEPENDENT HYPERPOLARIZATION; CORONARY-ARTERY; RELAXING FACTOR; CAROTID-ARTERY; GUINEA-PIG; RAT AORTA; ACETYLCHOLINE; ANGIOTENSIN;
Keywords:
apamin; experimental hypertension; mesenteric artery; nitric oxide; nitroprusside; L-NAME; potassium channels;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Kimura, K Wakayama Med Coll, Dept Med, Div Cardiol, Wakayama 6408156, Japan Wakayama Med Coll Wakayama Japan 6408156 kayama 6408156, Japan
Citazione:
K. Kimura et al., "Arterial relaxation mediated by endothelium-derived hyperpolarizing factorin hypertension induced by chronic inhibition of nitric oxide synthesis", CLIN EXP HY, 21(7), 1999, pp. 1203-1221

Abstract

The aim of this study was to evaluate arterial relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) during chronic inhibition of nitric oxide (NO) synthase. We measured the isometric tension of isolated mesenteric arteries of Wistar rats administered N-omega-nitro-L-arginine methyl ester (L-NAME, 100 mg/Kg/day) for 3 weeks. Relaxation to acetylcholine (ACh) was reduced in L-NAME treated rats (maximum relaxation, 52% versus 79%). After acute superfuison of 1x10(-4) M L-NAME, half the relaxation was inhibited in controls, while the relaxation was not changed in L-NAME treated rats. In contrast, relaxation to nitroprusside was normal in L-NAME treated rats. Superfusion of 1x10(-6) M apamin, which inhibits the effects of EDHF, reduced the relaxation. The relaxation inhibited by apamin was not significantly different between the two groups. These findings suggested that in endothelial cells, the synthesis of EDHF is unchanged during a chronic deficiency of relaxation influence of NO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 01:08:36