| Autor: |
Weissgarten, Joshua, Berman, Sylvia, Efrati, Shai, Rapoport, Micha, Modai, David, Cohn, Mirel, Aladjem, Mordechay, Galperin, Elena, Averbukh, Zhan |
| Předmět: |
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| Zdroj: |
Nephron Physiology; 2005, Vol. 101 Issue 1, p14-20, 7p |
| Abstrakt: |
Background/Aim: Hypertension induced by exaggerated sodium consumption accelerates the progression of renal failure. We investigated the effects of a high-sodium (HS) diet on the progression of renal failure in rats maintained normotensive by angiotensin-converting enzyme inhibition or AT-1 blockade. Methods: In 70 Sprague-Dawley rats, renal failure was induced by five-sixths nephrectomy. They were fed isocaloric normal-sodium (NS), low-sodium (LS), or HS diets. HS rats prone to develop hypertension were divided into three subgroups: treated to normotension by irbesartan (HS-1) or captopril (HS-2) or left untreated (HS-0). Results: All HS animals developed significant proteinuria which strongly correlated with the 24-hour sodium excretion. HS-0 rats demonstrated severe hypertension, rapid deterioration of the renal function, and 100% mortality after 3 weeks. In irbesartan-treated HS-1 rats, mortality and decline of the glomerular filtration rate were similar to those of normal- or low-sodium-fed animals (100% mortality after week 12). In captopril-treated HS-2 rats, glomerular filtration rate decline and mortality were significantly blunted as compared with all other groups (50% mortality after week 12). Conclusions: (1) In five-sixths-nephrectomized uremic rats maintained normotensive by either irbesartan or captopril, the rate of deterioration of the renal function was not aggravated by exaggerated sodium consumption. (2) In this experimental setting, captopril treatment yielded a better survival outcome as compared with irbesartan, despite the similar hypotensive effect. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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