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REDUCED FUNCTIONALITY OF RENIN‐ANGIOTENSIN‐ALDOSTERONE SYSTEM IN YOUNG RATS EXPOSED TO HIGH‐SALT DIET
Author(s) -
Crestani Sandra,
Garparotto Arquimedes,
Marques Maria Consuelo Andrade,
Sullivan Jennifer C.,
Webb R. Clinton,
Silva Santos Jose Eduardo
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1140.4
Subject(s) - medicine , endocrinology , aldosterone , renin–angiotensin system , angiotensin ii , bradykinin , blood pressure , weaning , chemistry , plasma renin activity , receptor
High salt (HS) intake is putatively associated with increased incidence and prevalence of hypertension. We hypothesized that HS diet (NaCl at 2, 4 or 8%) given from weaning for 6 weeks would impair the renin‐angiotensin system (RAS). After treatment, animals were anesthetized and the effects of angiotensin I (AI) and II (AII) at 3, 10 and 30 ρmol/kg, or bradykinin (BK; 3, 10 and 30 nmol/kg) on mean arterial pressure (MAP) were evaluated. Blood samples were used to measure the activity of angiotensin converting enzyme (ACE), circulating aldosterone and AII levels. HS intake did not increase MAP, but the responsiveness to AI was increased around 40 and 80% in HS 4 and 8% groups. The plasmatic activity of ACE augmented from 80 ± 2 (control) to 91 ± 3 nmol/min/mlin HS 8% group, while BK‐induced hypotension was reduced. The effects of AII were also increased in HS 8% group. Despite the enhanced ACE activity and responsiveness to exogenous AII, rats exposed to HS intake presented reduced levels of plasmatic AII and aldosterone, suggesting that regulatory changes in RAS system may, at least in young rats, counteract the beginning of hypertension elicited by excessive salt ingestion. Financial support: CAPES, CNPq and NIH.