EFFECTS OF DEOXYCORTICOSTERONE ACETATE (DOCA) AND ALDOSTERONE ON SAR(1)- ANGIOTENSIN-II BINDING AND ANGIOTENSIN-CONVERTING ENZYME BINDING-SITES IN BRAIN

1. It is known that regulation of salt appetite is a complex behavior controlled in the brain by interaction of mineralocorticoids (MC) and angiotensin II (ANGII). To investigate the effects of MC on ANGII rece ptors and ANGII synthesis, we have studied two models of salt appetite control. 2. In the first model, doses of DOCA sufficient to induce sa lt appetite of intact rats were given. In the second one, we studied t he effects of aldosterone (ALDO) in doses sufficient to suppress salt appetite developed by prior adrenalectomy (ADX). 3. Binding to ANGII r eceptors was determined in brain sections incubated with 3 nM [I-125]S ar(1) ANGII, exposed to [H-3]Hyperfilm with an optical density of auto radiograms measured by computerized densitometry. Sar(1)-ANGII binding was increased by DOCA treatment in the median preoptic nucleus (MnPO) and subfornical organ (SFO) but not in the paraventricular nucleus (P VN) in comparison to vehicle-treated rats. ALDO treatment was without effect on the MnPO but increased ANGII binding in the SFO and PVN. Nei ther hormone affected binding in the median eminence or anterior pitui tary (AP). 4. In contrast to effects on Sar(1)-ANGII binding in select ed areas, [I-125]351A binding to angiotensin-converting enzyme (ACE) w as unchanged by DOCA or ALDO administration in the SFO, caudate putame n, AP, or posterior pituitary. 5. These findings suggest that MC modul ation of the renin-angiotensin system is exerted at the central, and n ot at the pituitary level. ANGII receptors were modulated in a dose- a nd region-specific manner: while DOCA may promote their actions upon t he MnPO and SFO, ALDO actions may occur at the PVN and SFO. This mecha nism may not require increased generation of ANGII in the brain or pit uitary.