title: Dietary salt excess unmasks blunted aldosterone suppression and sodium retention in the stroke-prone phenotype of the spontaneously hypertensive rat.
abstract: OBJECTIVE
  The mechanisms underlying the accelerating effect of high salt intake on the development of vascular injury in the stroke-prone phenotype of spontaneously hypertensive rats (SHRSP) are still not clear. The aim of the present study was to determine whether young SHRSP can excrete a dietary excess of sodium and to characterize the associated hormonal responses.
  
  
  METHODS
  Sodium balance and hormonal parameters were studied during a 1-week high-salt diet (4% NaCl) in 6-week-old SHRSP (n = 84), in age-matched spontaneously hypertensive rats (SHR; n = 73) and in normotensive Wistar-Kyoto (WKY) rats (n = 52).
  
  
  RESULTS
  Baseline systolic blood pressure (SBP) was similar in SHR and SHRSP and did not change significantly during the high-salt diet. SBP also remained unchanged in WKY rats during the high-salt diet. Despite similar daily sodium intakes in the three groups during the diet, the response of urinary sodium excretion to sodium loading was reduced significantly in SHRSP compared with SHR or WKY rats (F = 4.09, P < 0.001). Plasma renin activity was suppressed significantly by high salt intake in each group to a comparable extent. Plasma aldosterone concentrations were also reduced significantly by sodium loading in all strains. However, a lesser degree of aldosterone suppression was observed in the SHRSP than in both SHR and WKY rats (F = 3.01, P < 0.01).
  
  
  CONCLUSIONS
  Young SHRSP show a blunted suppression of plasma aldosterone and a defective sodium excretion during high salt intake.
authors.affiliation: 1a Clinica Medica, 2a Facoltà di Medicina e Chirurgia, Università degli Studi Federico II, Naples, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Volpe
authors.forename: S
authors.initials: S
authors.lastname: Rubattu
authors.forename: D
authors.initials: D
authors.lastname: Ganten
authors.forename: I
authors.initials: I
authors.lastname: Enea
authors.forename: R
authors.initials: R
authors.lastname: Russo
authors.forename: G
authors.initials: G
authors.lastname: Lembo
authors.forename: A
authors.initials: A
authors.lastname: Mirante
authors.forename: G
authors.initials: G
authors.lastname: Condorelli
authors.forename: B
authors.initials: B
authors.lastname: Trimarco
mesh_terms: D000284:Administration, Oral; D000450:Aldosterone / Q000097:blood; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000235:genetics*; D004039:Diet, Sodium-Restricted; D006339:Heart Rate / Q000187:drug effects; D006728:Hormones / Q000097:blood; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology*; D010641:Phenotype; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology; D014556:Urine / Q000737:chemistry
chemical_list: D006728:Hormones; D000451:Mineralocorticoid Receptor Antagonists; D012965:Sodium Chloride; D000450:Aldosterone; D012964:Sodium