Mineralocorticoid treatment attenuates activation of oxytocinergic and vasopressinergic neurons by icv ANG II

Central oxytocin (OT) neurons limit intracerebroventricular (icv) ANG II-in duced NaCl intake. Because mineralocorticoids synergistically increase ANG II-induced NaCl intake, we hypothesized that mineralocorticoids may attenua te ANG II-induced activation of inhibitory OT neurons. To test this hypothe sis, we determined the effect of deoxycorticosterone (DOCA; 2 mg/day) on ic v ANG II-induced c-Fos immunoreactivity in OT and vasopressin (VP) neurons in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamu s and also on pituitary OT and VP secretion in male rats. DOCA significantl y decreased the percentage of c-Fos-positive (%c-Fos+) OT neurons in the SO N and PVN, both in the magnocellular and parvocellular subdivisions, and th e %c-Fos+ VP neurons in the SON after a 5-ng icv injection of ANG II. DOCA also significantly reduced the %c-Fos+ OT neurons in the SON after 10 ng AN G II and tended to attenuate 10 ng ANG II-induced OT secretion. However, th e %c-Fos+ OT neurons in DOCA-treated rats was greater after 10 ng ANG II, a nd DOCA did not affect the %c-Fos+ OT neurons in the PVN nor VP secretion o r c-Fos immunoreactivity in either the SON or PVN after 10 ng ANG II. DOCA also did not significantly alter the effect of intraperitoneal (ip) cholecy stokinin (62 mug) on %c-Fos+ OT neurons or of ip NaCl (2 ml of 2 M NaCl) on the %c-Fos+ OT and VP neurons. These findings indicate that DOCA attenuate s the responsiveness of OT and VP neurons to ANG II without completely supp ressing the activity of these neurons and, therefore, support the hypothesi s that attenuation of OT neuronal activity is one mechanism by which minera locorticoids enhance NaCl intake.