title: High-salt diet increases plasma adiponectin levels independent of blood pressure in hypertensive rats: the role of the renin-angiotensin-aldosterone system.
abstract: BACKGROUND
  High sodium intake is associated with increased risk of end-organ damage, independent of blood pressure (BP) levels. The protective peptide adiponectin may play a role in the pathogenesis of hypertension and particularly in salt-loaded conditions. Furthermore, increased adiponectin levels were observed in salt-loaded conditions. However, there is little information on the direct effect of high-salt diet on plasma adiponectin. The aim of the present study was to examine the effect of high-salt diet on adiponectin levels in Sprague-Dawley rats and explore the mechanisms that regulate adiponectin levels under salt loading.
  
  
  METHODS
  Sprague-Dawley rats were fed either standard chow diet or medium or high sodium diet for 5 weeks. BP and plasma adiponectin were measured at baseline and during the study. In additional studies the same protocol was repeated with the addition of clonidine, telmisartan, hydralazine or eplerenone.
  
  
  RESULTS
  High-salt diet increased systolic BP, suppressed plasma aldosterone levels and attenuated body weight gain. Five weeks of salt loading increased plasma adiponectin levels in a dose-dependent manner (medium salt and high salt were 47 and 93% higher than control, respectively, P < 0.05). Hydralazine and clonidine attenuated salt-induced BP increase but did not attenuate the increase in adiponectin levels whereas, telmisartan, an angiotensin receptor blocker, and eplerenone, an aldosterone blocker, attenuated both the increase in BP and in adiponectin levels.
  
  
  CONCLUSIONS
  High salt intake increases adiponectin levels independent of the increase in BP. This effect is mediated through the renin-angiotensin-aldosterone system.
authors.affiliation: Hypertension Unit, Chaim Sheba Medical Center, Tel Hashomer, Israel. yehuda.kamari@sheba.health.gov.il
authors.forename: Yehuda
authors.initials: Y
authors.lastname: Kamari
authors.forename: Nir
authors.initials: N
authors.lastname: Shimoni
authors.forename: Faina
authors.initials: F
authors.lastname: Koren
authors.forename: Edna
authors.initials: E
authors.lastname: Peleg
authors.forename: Yehonatan
authors.initials: Y
authors.lastname: Sharabi
authors.forename: Ehud
authors.initials: E
authors.lastname: Grossman
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001562:Benzimidazoles / Q000494:pharmacology; D001565:Benzoates / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D003000:Clonidine / Q000494:pharmacology; D000077545:Eplerenone; D006830:Hydralazine / Q000494:pharmacology; D006973:Hypertension / Q000097:blood* / Q000188:drug therapy; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013148:Spironolactone / Q000031:analogs & derivatives / Q000494:pharmacology; D000077333:Telmisartan
chemical_list: D052242:Adiponectin; D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001565:Benzoates; D017673:Sodium Chloride, Dietary; D006830:Hydralazine; D013148:Spironolactone; D000077545:Eplerenone; D003000:Clonidine; D000077333:Telmisartan