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Central mineralocorticoid receptor blockade reduces sodium appetite in rats: new evidence for an old effect
Author(s) -
Formenti Silmara,
Schoorlemmer Guus,
Menani José V.,
Colombari Eduardo
Publication year - 2010
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.24.1_supplement.1025.13
Subject(s) - endocrinology , sodium , medicine , aldosterone , mineralocorticoid receptor , mineralocorticoid , chemistry , furosemide , appetite , ventricle , antagonist , receptor , organic chemistry
In a previous study we showed that chronic infusion of the mineralocorticoid hormone aldosterone into the fourth ventricle (4V) induces robust dose‐dependent daily sodium intake. In the present study we investigated the effects of the mineralocorticoid receptor (MR) antagonist, RU 28318, injected into the 4V or lateral ventricle (LV) on sodium intake induced by 24 h of sodium depletion (treatment with furosemide, 20 mg/kg b.w., s.c., followed by 24 h of sodium deficient diet), 9 days of sodium deficient diet (0.005% Na + ) or chronic treatment with deoxycorticosterone acetate (DOCA, 2 mg/day, s.c. for 7 days). Male Wistar Hannover rats (280–350 g, n=4–7/group) with stainless steel guide cannulas implanted into the 4V or into the LV were used. RU 28318 (100 ng) into the 4V reduced 0.3 M NaCl intake induced by 24 h of sodium depletion (6±1 vs. vehicle: 12±2 mL/2 h) or by sodium deficient diet (1±1 vs. vehicle: 9.5±3 mL/2 h). However, injection of RU 28318 (100 ng) into the LV did not affect sodium intake induced by 24 h of sodium depletion (15±3 vs. vehicle: 15±3 mL/2h). RU 28318 (500 ng) into the 4V also produced no effect on sodium intake induced by DOCA (14±3 vs. vehicle: 11±2 mL/2 h). These data reinforce findings suggesting that hindbrain MRs are involved on aldosterone‐induced sodium appetite. However, it seems they are not involved on DOCA‐induced sodium intake. Supported by: FAPESP, CNPq, CAPES.