title: Increased Dietary Salt Changes Baroreceptor Sensitivity and Intrarenal Renin-Angiotensin System in Goldblatt Hypertension.
abstract: BACKGROUND
  Renovascular hypertension (2-kidney 1-clip model (2K1C)) is characterized by renin-angiotensin system (RAS) activation. Increased Angiotensin II (AngII) leads to sympathoexcitation, oxidative stress, and alterations in sodium and water balance.
  
  
  OBJECTIVE
  The aim of this study was to evaluate whether a discrete increase in sodium chloride intake in 2K1C rats leads to changes in cardiovascular and autonomic function, oxidative stress, and renin angiotensin aldosterone system.
  
  
  METHODS
  After 4 weeks of induction of hypertension, rats were fed a normal sodium diet (0.4% NaCl) or a high-sodium diet (2% NaCl) for 2 consecutive weeks. Experiments were carried out for 6 weeks after clipping. Mean arterial pressure (MAP), renal sympathetic nerve activity (rSNA), arterial baroreflex control of rSNA, and heart rate (HR) were assessed. Thiobarbituric acid reactive substances and glutathione were measured as indicators of systemic oxidative stress. Angiostensin-converting enzyme (ACE), ACE2, and angiotensinogen were evaluated in clipped and unclipped kidneys as also urinary angiotensinogen and plasma renin activity. Angiotensinogen, plasma renin activity (PRA) and angiotensin-converting enzyme (ACE) and ACE2 in clipped and unclipped kidneys were evaluated.
  
  
  RESULTS
  High-sodium diet did not change systemic oxidative stress, and basal values of MAP, HR, or rSNA; however, increased renal (-0.7±0.2 vs. -1.5±0.1 spikes/s/mm Hg) and cardiac (-0.9±0.14 vs. -1.5±0.14 bpm/mm Hg) baroreceptor reflex sensitivity in 2K1C rats. Although there was no alteration in PRA, a high-salt diet significantly decreased urinary angiotensinogen, ACE, and ACE2 expressions in the clipped and unclipped kidneys.
  
  
  CONCLUSIONS
  Increased arterial baroreceptor control associated with a suppression of the intrarenal RAS in the 2K1C rats on high-salt diet provide a salt-resistant effect on hypertension and sympathoexcitation in renovascular hypertensive rats.
authors.affiliation: Cardiovascular Division-Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil.
authors.forename: Caroline G
authors.initials: CG
authors.lastname: Shimoura
authors.affiliation: Cardiovascular Division-Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil.
authors.forename: Gisele S
authors.initials: GS
authors.lastname: Lincevicius
authors.affiliation: Cardiovascular Division-Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil.
authors.forename: Erika E
authors.initials: EE
authors.lastname: Nishi
authors.affiliation: Heart Institute (InCor) University of São Paulo Medical School, São Paulo, São Paulo, Brazil.
authors.forename: Adriana C C
authors.initials: AC
authors.lastname: Girardi
authors.affiliation: Department of Biological Sciences, Universidade Federal de São Paulo, Diadema, Brazil.
authors.forename: Karin A
authors.initials: KA
authors.lastname: Simon
authors.affiliation: Cardiovascular Division-Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil.
authors.forename: Cassia T
authors.initials: CT
authors.lastname: Bergamaschi
authors.affiliation: Cardiovascular Division-Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil; ruy.camposjr@unifesp.br.
authors.forename: Ruy R
authors.initials: RR
authors.lastname: Campos
mesh_terms: D000818:Animals; D006339:Heart Rate; D006978:Hypertension, Renovascular / Q000503:physiopathology* / Q000652:urine; D008297:Male; D018384:Oxidative Stress; D011311:Pressoreceptors / Q000187:drug effects / Q000503:physiopathology*; D017208:Rats, Wistar; D012084:Renin-Angiotensin System; D012965:Sodium Chloride / Q000009:adverse effects; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*
chemical_list: D017673:Sodium Chloride, Dietary; D012965:Sodium Chloride
keywords: baroreflex dysfunction; blood pressure; high-sodium intake; hypertension; renal sympathetic nerve activity; renin angiotensin aldosterone system; renovascular hypertension.