Aldosterone Acts in the Nucleus of the Solitary Tract to Alter Stress Responsiveness

Abstract

Aldosterone (aldo) acts at brain mineralocorticoid receptors (MR) to increase arterial pressure. We hypothesized that activation of MR selectively within the Nucleus Tractus Solitarius (NTS), a key circulatory control center, would enhance the cardiovascular response restraint stress. Mean arterial pressure (MAP) was measured by radiotelemetry in adult male Sprague–Dawley rats. Chronic elevations in aldo levels within the NTS were achieved by implanting pellets of 1% aldo over the NTS (n=4). Sham pellets were made of silastic (n=4). All rats were subjected to 60 min of restraint stress daily for 11 days. On day 12 they were exposed to a novel stress by placing them in 1 cm of room temp water for 15 min. Aldo did not alter baseline MAP. Aldo attenuated the integrated MAP response to restraint stress on the first day (990±50 mmHg/60 min vs 1510± 82 mmHg/60 min, aldo vs sham, P=0.002). The MAP response to the final restraint stress was not significantly affected by aldo. With water stress, the integrated MAP response was enhanced in the aldo‐ vs. the sham‐treated rats (416±14 mmHg/15 min vs. 332±32 mmHg/15 min, P=0.054). Compared with the sham rats, the aldo‐treated rats gained less weight during the period of chronic stress (2±5 gm, n=4 vs. 24±7 gm, n=3, P=0.04). We conclude that aldosterone acts in the NTS to influence stress responsiveness. Support: NIH#HL 076807, AHA#GRNT 4460047.