Effect of endothelin blockade on pressure natriuresis in nitric oxide‐deficient hypertensive rats
作者:
Lourdes Fortepiani,
Jean Janvier,
M Ortíz,
Noemí Atucha,
Joaquín García-Estañ,
期刊:
Journal of Hypertension
(OVID Available online 1999)
卷期:
Volume 17,
issue 2
页码: 287-291
ISSN:0263-6352
年代: 1999
出版商: OVID
关键词: arterial hypertension;kidney;renal hemodynamics;renal sodium handling
数据来源: OVID
摘要:
ObjectiveChronic inhibition of nitric oxide synthesis has been shown to cause arterial hypertension and an important blunting of the pressure diuresis and natriuresis response. The mechanisms mediating these abnormalities are not completely established. We therefore studied the effects of endothelin on these alterations.Materials and methodsPressure diuretic and natriuretic relationships were evaluated in rats treated chronically (3 weeks) with the nitric oxide synthesis inhibitor Nω-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg per day), alone or in combination with bosentan sodium salt (acute treatment: 10 mg/kg, intravenously; chronic treatment: 10 mg/kg per day).ResultsChronic treatment with L-NAME significantly elevated mean arterial pressure (143.7 ± 2.8 mmHg versus 102.8 ± 1.6 in controls), reduced the glomerular filtration rate and renal blood flow and shifted the pressure diuretic and natriuretic responses to the right. Treatment with bosentan, either acute or chronically, did not attenuate the arterial hypertension of the L-NAME-treated rats but normalized the glomerular filtration rate and renal blood flow. In spite of the normalization of renal hemodynamics, the pressure diuretic and natriuretic responses of the bosentan-treated groups were not normalized, although chronic bosentan significantly improved the pressure natriuretic response.ConclusionsThese results indicate that endothelin participates in the renal hemodynamic and excretory alterations that follow chronic inhibition of nitric oxide synthesis. However, the arterial hypertension is not mediated by endothelin activation.
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