title: Control of hypertension with captopril affords better renal protection as compared with irbesartan in salt-loaded uremic rats.
abstract: OBJECTIVE
  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.
authors.affiliation: Nephrology Division, Assaf Harofeh Medical Center, Affiliated to Sackler Faculty of Medicine, Tel Aviv University, Zerifin, Israel. Weissgarten@asaf.health.gov.il
authors.forename: Joshua
authors.initials: J
authors.lastname: Weissgarten
authors.forename: Sylvia
authors.initials: S
authors.lastname: Berman
authors.forename: Shai
authors.initials: S
authors.lastname: Efrati
authors.forename: Micha
authors.initials: M
authors.lastname: Rapoport
authors.forename: David
authors.initials: D
authors.lastname: Modai
authors.forename: Mirel
authors.initials: M
authors.lastname: Cohn
authors.forename: Mordechay
authors.initials: M
authors.lastname: Aladjem
authors.forename: Elena
authors.initials: E
authors.lastname: Galperin
authors.forename: Zhan
authors.initials: Z
authors.lastname: Averbukh
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000008:administration & dosage; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage; D000818:Animals; D000959:Antihypertensive Agents / Q000008:administration & dosage; D001713:Biphenyl Compounds / Q000008:administration & dosage*; D002216:Captopril / Q000008:administration & dosage*; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006977:Hypertension, Renal / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D000077405:Irbesartan; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017673:Sodium Chloride, Dietary / Q000378:metabolism; D015996:Survival Rate; D013777:Tetrazoles / Q000008:administration & dosage*; D016896:Treatment Outcome; D014511:Uremia / Q000150:complications / Q000209:etiology / Q000503:physiopathology
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D001713:Biphenyl Compounds; D017673:Sodium Chloride, Dietary; D013777:Tetrazoles; D002216:Captopril; D000077405:Irbesartan