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Titolo:
Role of nitric oxide in regional blood flow in angiotensin II-induced hypertensive rats
Autore:
Nishiyama, A; Fujisawa, Y; Fukui, T; Rahman, M; Kondo, N; Ogawa, Y; Li, FZ; Zhang, GX; Kimura, S; Abe, Y;
Indirizzi:
Kagawa Med Univ, Dept Pharmacol, Miki, Kagawa 7610793, Japan Kagawa Med Univ Miki Kagawa Japan 7610793 ol, Miki, Kagawa 7610793, Japan Kagawa Med Univ, Res Equipment Ctr, Miki, Kagawa 7610793, Japan Kagawa MedUniv Miki Kagawa Japan 7610793 tr, Miki, Kagawa 7610793, Japan
Titolo Testata:
Hypertension research
fascicolo: 4, volume: 24, anno: 2001,
pagine: 421 - 427
Fonte:
ISI
Lingua:
ENG
Soggetto:
AFFERENT ARTERIOLAR REACTIVITY; RENAL MICROCIRCULATION; DEPENDENT HYPERTENSION; CONSCIOUS RATS; HEMODYNAMICS; EXPRESSION; INHIBITION; PRESSURE; EXERCISE; RELEASE;
Keywords:
angiotensin II; nitric oxide; hypertension; regional blood flow; (+/-)-(E)-4-ethyl-2-[(E)-hydroxy-imino]-5-nitro-3-hexenamide (FK409);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Nishiyama, A Kagawa Med Univ, Dept Pharmacol, 1750-1 Ikenobe, Miki, Kagawa7610793, Japan Kagawa Med Univ 1750-1 Ikenobe Miki Kagawa Japan 7610793 apan
Citazione:
A. Nishiyama et al., "Role of nitric oxide in regional blood flow in angiotensin II-induced hypertensive rats", HYPERTENS R, 24(4), 2001, pp. 421-427

Abstract

The present study was designed to evaluate the contribution of nitric oxide (NO) to regional hemodynamics during the early phase of angiotensin II (Ang II)-induced hypertension. The responses of regional blood flow to chronic NO synthase inhibition with N-G-nitro-L-arginine methyl ester (L-NAME) were assessed using radioactive microspheres in conscious Ang II-Infused hypertensive rats. Ang II-infused rats (270 ng/kg/min, subcutaneously for 12 days: n=11) showed higher mean arterial pressure (MAP: 153+/-4 mmHg) and total peripheral resistance (TPR: 1.61+/-0.06 mmHg/min/ml), and lower cardiac output (CO: 102+/-3 mi/min) than vehicle-infused normotensive rats (115+/-2 mmHg, 0.96+/-0.05 mmHg/min/ml and 130+/-7 ml/min, n=11, respectively). The blood flow rates in the brain, spleen, large intestine and skin were significantly reduced in Ang II-infused rats compared with vehicle-infused rats, while those in the lung, heart, liver, kidney, adrenal gland, small intestine, and skeletal muscle were similar. Treating Ang II-infused rats with L-NAME (75 mg/l in drinking water for 10 days, n=11) resulted in higher MAP (166+/-6 mmHg) and TPR (1.89+/-0.18 mmHg/min/ml) and lower CO (87+/-7 ml/min)than untreated Ang II-infused rats. L-NAME-treated Ang II-infused rats showed widespread increases in regional vascular resistance and reduced blood flow rates in the kidney (3.81+/-0.27 ml/min/g) and skeletal muscle (0.20+/-0.03 ml/min/g) compared with untreated Ang II-infused rats (6.88+/-0.27 and 0.33+/-0.04 ml/min/g, respectively). However, there were no significant differences in the flow rates of other organs investigated between these animals. An NO donor, (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409: 30 mug/kg/min, i.v.), significantly decreased MAP (110+/-6 mmHg) and TPR (1.23+/-0.18 mmHg/min/ml) without significant changes in CO (89+/-9 ml/min) in L-NAME-treated Ang II-infused rats. Furthermore, FK409 partially reversed blood flow rates in the kidney (4.72+/-0.40 ml/min/g) and skeletal muscle (0.25+/-0.02 ml/min/g) in these animals. These results suggest that NO counteracts, at least in part, the vasoconstrictor effects of elevated Ang II levels in renal and skeletal muscle vascular beds, and is an important modulator in the regulation of blood flow to these organs during thedevelopment of Ang II-induced hypertension.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 13:46:24