Animal studies suggest that acute and chronic aldosterone administration impairs baroreceptor/baroreflex responses. We tested the hypothesis that aldosterone impairs baroreflex control of cardiac period [cardiovagal baroreflex sensitivity (BRS)] and muscle sympathetic nerve activity (MSNA: sympathetic BRS) in humans. Twenty young (25±1 years old, mean±SE) adults were examined in this randomized, double-blinded, and placebo-controlled study. BRS was determined using the modified Oxford technique (bolus infusion of nitroprusside followed 60 s later by bolus infusion of phenylephrine) in triplicate before (Pre) and 30-min after (Post) beginning aldosterone (experimental; 12 pmol/kg/min; n=10) or saline infusion (control; n=10). BRS was quantified from the RR interval- systolic blood pressure (BP) (cardiovagal BRS) and MSNA- diastolic BP (sympathetic BRS) relations. Aldosterone infusion increased serum aldosterone levels ~4-fold (P<0.05) and decreased (P<0.05) cardiovagal (19.0±2.3 vs. 15.6±1.7 ms/mmHg Pre and Post, respectively) and sympathetic BRS (-4.4±0.4 vs. -3.0±0.4 au/beat/mmHg). In contrast neither cardiovagal (19.3±3.3 vs. 20.2±3.3 ms/mmHg) nor sympathetic BRS (-3.8±0.5 vs. -3.6±0.5 au/beat/mmHg) were altered (Pre vs. Post) in the control group. BP, heart rate, and MSNA at rest were similar in experimental and control subjects before and after the intervention. Neural and cardiovascular responses to a cold pressor test and isometric handgrip to fatigue were unaffected by aldosterone infusion (n=6). These data provide direct experimental support for the concept that aldosterone impairs baroreflex function (cardiovagal and sympathetic BRS) in humans. Therefore, aldosterone may be an important determinant/modulator of baroreflex function particularly in disease states associated with elevated circulating levels of aldosterone.