Pressure natriuresis following acute and chronic inhibition of nitric oxide synthase in rats
| Autor: | Robert L. Kline, G. R. Guarasci |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Physiology Hydrostatic pressure Natriuresis Blood Pressure Arginine Kidney Renal Circulation Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Reference Values Physiology (medical) Internal medicine medicine Animals biology Chemistry Rats Filtration fraction Nitric oxide synthase NG-Nitroarginine Methyl Ester Blood pressure medicine.anatomical_structure Endocrinology Renal blood flow Hypertension biology.protein Nitric Oxide Synthase Glomerular Filtration Rate |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 270:R469-R478 |
| ISSN: | 1522-1490 0363-6119 |
| Popis: | Nitric oxide has been suggested to be an essential mediator of pressure natriuresis. To investigate this hypothesis, the effect of acute or chronic inhibition of nitric oxide synthase on pressure natriuresis and renal interstitial hydrostatic pressure was studied in anesthetized Sprague-Dawley rats with fixed neural and hormonal influences on the kidney. Both acute infusion (10 micrograms.kg-1.min-1 iv) and chronic administration (50 mg.kg-1.day-1 for 7 days in drinking water) of NG-nitro-L-arginine methyl ester (L-NAME) resulted in significantly increased mean arterial pressure, a 30% decrease in renal blood flow, and no change in glomerular filtration rate when compared with values in control rats. Pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium excretion curves in L-NAME-treated rats were shifted to a higher pressure (by approximately 25 mmHg) when compared with those in control rats. The relationship between renal artery pressure and renal interstitial hydrostatic pressure was shifted similarly in L-NAME-treated rats. Acute administration of L-arginine completely reversed the renal effects of chronic L-NAME. These data indicate that, at the doses used in this study, both acute and chronic inhibition of nitric oxide synthase decreased the ability of the kidney to excrete sodium at least in part by a hemodynamic mechanism leading to an increased filtration fraction and a decreased renal interstitial pressure. The parallel shift of the pressure-natriuresis curve to a higher pressure suggests that nitric oxide is an important modulator but not an essential mediator of the pressure natriuresis. |
| Databáze: | OpenAIRE |
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