title: Alterations in aldosterone and angiotensin II levels in salt-induced hypertension.
abstract: Several studies have demonstrated that plasma renin-angiotensin activity is reduced in rats administered a high salt diet. We evaluated changes in plasma and tissue levels of aldosterone (ALDO) and angiotensin II (A-II), as well as the reduced-to-oxidized glutathione ratio. Male Dahl salt-sensitive (SS) rats were placed on either a high-salt (8% NaCl; HS) or a normal-salt (0.3% NaCl; NS) diet for 3 weeks. Prior to and weekly on the diets, systolic blood pressure was measured by tail cuff plethysmography. Levels of A-II and ALDO in plasma, heart, and kidney were analyzed by enzyme immunoassay. Reduced and oxidized gluthatione were simultaneously measured by HPLC fluorescence detection. Heart and kidney tissues were prepared for histological analysis. Systolic blood pressure in animals on a HS diet was significantly elevated above that of those on a NS diet. High salt caused a reduction in both plasma A-II and ALDO levels; while their levels in the heart and kidney were increased. Exposure to a high-salt diet led to the enlargement of both heart and kidney. The reduced-to-oxidized glutathione ratio in plasma, heart and kidney was lowered by exposure to a HS diet. Kidneys from animals on a high-salt diet showed fibroid necrosis associated with wrinkling and thickening of the glomerular capillary wall, while hearts were hypertrophic. Taken together, high dietary salt induces inappropriate activation of the local renin-angiotensin-aldosterone systems. Tissue levels of angiotensin II and aldosterone may be more reflective of the severity of vascular maladaptations than are plasma levels, and may play a greater role in the maintenance of hypertension.
authors.affiliation: Department of Pharmacology, Morehouse School of Medicine, Atlanta, GA 30310-1495, USA. bayorh@msm.edu
authors.forename: Mohamed A
authors.initials: MA
authors.lastname: Bayorh
authors.forename: A A
authors.initials: AA
authors.lastname: Ganafa
authors.forename: N
authors.initials: N
authors.lastname: Emmett
authors.forename: R R
authors.initials: RR
authors.lastname: Socci
authors.forename: D
authors.initials: D
authors.lastname: Eatman
authors.forename: I L
authors.initials: IL
authors.lastname: Fridie
mesh_terms: D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D006321:Heart / Q000033:anatomy & histology; D006339:Heart Rate; D006973:Hypertension / Q000378:metabolism*; D007668:Kidney / Q000033:anatomy & histology / Q000378:metabolism; D008297:Male; D008638:Mesenteric Arteries / Q000033:anatomy & histology / Q000378:metabolism; D008833:Microcirculation; D009206:Myocardium / Q000378:metabolism; D009929:Organ Size; D051381:Rats; D020303:Rats, Inbred Dahl; D012084:Renin-Angiotensin System / Q000502:physiology; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*
chemical_list: D017673:Sodium Chloride, Dietary; D000804:Angiotensin II; D000450:Aldosterone; D005978:Glutathione; D019803:Glutathione Disulfide