CENTRAL EFFECT OF ANGIOTENSIN-III ON CAUDAL HYPOGLOSSAL NEURONS IN RATS

We communicated the central effect of angiotensin III (ANG III), a pot ent signal for extracellular dehydration, on single neurons in the cau dal hypoglossal nucleus of Sprague-Dawley rats anesthetized with pento barbital sodium. A significant number (121 of 168) of caudal hypogloss al neurons responded to intracerebroventricular application of ANG III (80 or 160 pmol), with either an increase (n = 83) or decrease (n = 3 8) in their spontaneous discharge. These effects of ANG III were signi ficantly reversed by intracerebroventricular application of the nonpep tide angiotensin AT(1) receptor antagonist losartan (40 nmol), but not by the AT(2) antagonist, PD-123319. The hypoglossal neuronal response s to repeated administration of ANG III (80 pmol), delivered at an int erval less than or equal to 18 min, exhibited acute tachyphylaxis. Int racerebroventricular administration of the cholinergic dipsogen, carba chol (50 ng), or the osmotic stimulant, hypertonic saline (0.5 M), als o elicited responses in ANG III-responsive hypoglossal neurons. These results suggest that neurons in the caudal hypoglossal nucleus may ser ve as the final common pathway for extracellular and, possibly, intrac ellular thirst in the rat. Furthermore, it is likely that the action o f ANG III is mediated by the AT(1) subtype of angiotensin receptors.