Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/55897
Type: Artigo
Title: Chronic inhibition of nitric-oxide synthesis - a new model of arterial-hypertension
Title Alternative: 
Author: Ribeiro, M.O.
Lovisolo, S.M.
De Nucci, G.
Antunes, E.
Zatz, R.
Abstract: Recent studies have indicated that acute inhibition of nitric oxide biosynthesis in the rat promotes arterial hypertension and renal vasoconstriction. We evaluated the renal and systemic effects of 4-6 weeks of nitric oxide blockade in Munich-Wistar rats receiving the nitric oxide inhibitor nitro-L-arginine orally. Age-matched untreated rats were used as controls. In an additional seven rats, nitric oxide blockade was carried out in conjunction with oral administration of the novel angiotensin II antagonist losartan potassium. Tail-cuff pressure rose progressively in nitro-L-arginine-treated rats, reaching 164+/-6 mm Hg at 4-6 weeks, compared with 108+/-3 mm Hg in controls. In rats concomitantly receiving losartan, tail-cuff pressure reached 125+/-6 mm Hg, still elevated compared with rats receiving losartan alone (98+/-3 mm Hg). Nitro-L-arginine-treated rats presented marked renal vasoconstriction and hypoperfusion, as well as a 30% fall in glomerular filtration rate and a 39% increase in filtration fraction. Treatment with Losartan normalized glomerular filtration rate, but not filtration fraction or renal vascular resistance. Plasma renin activity was elevated after nitro-L-arginine treatment. Renal histological examination revealed widespread arteriolar narrowing, focal arteriolar obliteration, and segmental fibrinoid necrosis in the glomeruli. In a separate group of rats, nitro-L-arginine administered for 1 week induced hypertension that was partially reversed by acute L-arginine, but not D-arginine or L-glycine, infusions. We conclude that chronic nitric oxide blockade may constitute a new model of severe arterial hypertension. Activation of the renin-angiotensin system may account, at least in part, for the vasoconstrictor activity after such inhibition
metadata.dc.description.abstractalternative: 
Subject: Pressão sanguínea
Óxido nítrico
Country: Estados Unidos
Editor: American Heart Association
Citation: Hypertension. Amer Heart Assoc, v. 20, n. 3, n. 298, n. 303, 1992.
Rights: fechado
Identifier DOI: 10.1161/01.HYP.20.3.298
Address: https://www.ahajournals.org/doi/10.1161/01.HYP.20.3.298
Date Issue: 1992
Appears in Collections:FCM - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
A1992JL73300004.pdf2.34 MBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.