Both suppression of sympathetic activity (SA) by chronic electrical activation of the carotid baroreflex (BA) and renal denervation (RDX) abolish obesity-induced hypertension (HT), which is mediated by increased SA. Evidence in support of a sympathetic component to aldosterone (Aldo) HT is equivocal. Therefore, at the same stimulation parameters in each dog, cardiovascular responses to 7 days of BA were determined in 9 dogs before (no HT) and after induction of HT by infusion of Aldo for 14 days (12μg/kg/day), which increased plasma levels ~ 10-fold (control= 4.3±0.4 ng/dL). 3 dogs with Aldo HT were subjected to RDX. Aldo HT was associated with increases in plasma osmolality (293±1 to 297±1 mOsm/kg) and [vasopressin] (AVP, Table), marked polydipsia (241± 90 to 2,380 ± 382 mL/day), hypokalemia (4.2±0.1 to 2.3±0.1 mmol/L), and suppression of plasma renin activity, but no significant changes in plasma [norepinephrine] (NE, Table). MAP (mmHg), NE (pg/mL), and AVP (pg/mL) responses to BA:
*P<0.05 vs Control
Plasma [NE] decreased with BA during both no HT and Aldo HT, indicating suppression of SA, but MAP lowering was appreciably diminished during Aldo HT. In contrast, there was no lowering of MAP after RDX. There were no significant changes in plasma osmolality, drinking, or [AVP] during BA. These findings indicate that classic renal mineralocorticoid mechanisms, not increased SA, account for the initial progression of HT produced by pathophysiological circulating levels of Aldo. Further, they show that chronic stimulation of baroreceptors afferents has differential central effects to suppress SA without altering control of plasma osmolality by suppressing thirst or AVP secretion.