EFFECT OF INTRAVENOUS CAPTOPRIL ON C-FOS EXPRESSION INDUCED BY SODIUMDEPLETION IN NEURONS OF THE LAMINA TERMINALIS

Peripheral administration of the angiotensin converting enzyme (ACE) i nhibitor, captopril, and the central infusion of sarile, an angiotensi n II (Ang II) receptor antagonist, were used to evaluate the role of r enal and brain generated Ang II in sodium depletion-induced production of Fos in cells of the subfornical organ (SFO) and organum vasculosum lamina terminalis (OVLT). Pretreatment with intravenous captopril (10 0 mg/kg) significantly inhibited the c-fos expression induced by sodiu m depletion in the SFO and OVLT. In contrast, continuous intracerebrov entricular infusion of sarile (22.5 mu g/4.5 h, 5 mu l/h) did not affe ct the expected pattern of c-fos expression observed in both nuclei, 4 h after peritoneal dialysis. These results show that systemic interfe rence with the angiotensin system of renal origen by captopril inhibit ed the production of Fos induced by sodium depletion in cells of the S FO and OVLT. These findings are consistent with the hypothesis that a rise in peripheral Ang II levels, triggered by sodium deficiency, coul d be an important mediator of the physiological and behavioral respons es that lead to the restoration of sodium balance. In addition, this s tudy suggests that increased circulating Ang II levels in response to body sodium deficit can directly stimulate neural pathways in the SFO and OVLT. (C) 1997 Elsevier Science Inc.