Weissgarten Joshua, Berman Sylvia, Efrati Shai, Rapoport Micha, Modai David, Cohn Mirel, Aladjem Mordechay, Galperin Elena, Averbukh Zhan
Nephrology Division, Assaf Harofeh Medical Center, Affiliated to Sackler Faculty of Medicine, Tel Aviv University, Zerifin, Israel.
Nephron Physiol. 2005;101(1):p14-20. doi: 10.1159/000086037. Epub 2005 May 27.
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.
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).
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).
(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.
背景/目的：过量摄入钠所致的高血压会加速肾衰竭的进展。我们研究了高钠（HS）饮食对通过血管紧张素转换酶抑制或AT-1阻断维持血压正常的大鼠肾衰竭进展的影响。
在70只Sprague-Dawley大鼠中，通过切除六分之五的肾脏诱导肾衰竭。给它们喂食等热量的正常钠（NS）、低钠（LS）或HS饮食。易患高血压的HS大鼠分为三个亚组：用厄贝沙坦（HS-1）或卡托普利（HS-2）治疗使血压正常，或不进行治疗（HS-0）。
所有HS动物均出现明显蛋白尿，且与24小时钠排泄量密切相关。HS-0大鼠表现出严重高血压、肾功能迅速恶化，3周后死亡率达100%。在厄贝沙坦治疗的HS-1大鼠中，死亡率和肾小球滤过率下降与正常或低钠饮食的动物相似（第12周后死亡率为100%）。在卡托普利治疗的HS-2大鼠中，与所有其他组相比，肾小球滤过率下降和死亡率明显降低（第12周后死亡率为50%）。
（1）在通过厄贝沙坦或卡托普利维持血压正常的六分之五肾切除的尿毒症大鼠中，过量摄入钠不会加重肾功能恶化速度。（2）在本实验环境中，尽管卡托普利和厄贝沙坦降压效果相似，但卡托普利治疗的生存结局优于厄贝沙坦。
