OBJECTIVETo reveal the nongenomic effect of aldosterone on the regulation of sodium intake in the nucleus tractus solitarius (NTS) and the role of central nucleus of the amygdala (CeA) in regulating this effect.

METHODSAdult male SD rats were divided into four groups and underwent operations to induce bilateral CeA electrolytic lesions (400 μA, 25 s; =28), bilateral sham CeA lesions (=28), unilateral CeA lesions (=28), or unilateral sham CeA lesions (=26). After 3 days of recovery, the rats received implantation of a stainless steel 23-gauge cannula wih two tubes into the NTS followed by a recovery period of 7 days. The rats in each group were then divided into two subgroups for microinjection of aldosterone (50 ng/μL) or control solution in the NTS, and the cumulative intake within 30 min of 0.3 mol/L NaCl solution was recorded for each rat.

RESULTSBilateral CeA lesions (3 days) eliminated the increased 0.3 mol/L NaCl intake induced by aldosterone microinjected into the NTS (0.3±0.04 mL in CeA lesion group 1.3±0.3 mL in sham lesion group). Unilateral CeA lesion (3 days) reduced aldosterone-induced increase of NaCl intake in the first 15 min ( < 0.05) but not in 15-30 min ( > 0.05). In rats with sham lesions, aldosterone (50 ng/μL) still induced a significant increase in NaCl intake[1.3±0.3 mL 0.25±0.02 mL in the control group; F (3, 224)=24.0, < 0.05].

CONCLUSIONSThe regulation of sodium intake by aldosterone is subjected to descending facilitatory modulation by the bilateral CeA, and CeA integrity is essential for aldosterone to execute the nongenomic effect in regulating rapid sodium intake.