Alpha-adrenergic agonists inhibit the dipsogenic effect of angiotensin IT by their stimulation of atrial natriuretic peptide release

Angiotensin II (ANG-II) and atrial natriuretic peptide (ANP) have opposing actions on water and salt intake and excretion. Within the brain ANP inhibi ts drinking induced by ANG-II and blocks dehydration-induced drinking known to be caused by release of ANG-ZI. Alpha-adrenergic agonists are known to release ANP and antagonize ANG II-induced drinking. We examined the hypothe sis that a. agonists block ANG-II-induced drinking by stimulating the relea se of ANP from ANP-secreting neurons (ANPergic neurons) within the brain th at inhibit the effector neurons stimulated by ANG-II to induce drinking. In jection of ANG-II (12.5 ng) into the anteroventral region of the third vent ricle (AV3V) at the effective dose to increase water intake increased plasm a ANP concentrations (P<0.01) within 5 min. As described before, previous i njection of phenylephrine (an <alpha>(1)-adrenergic agonist) or clonidine ( an alpha (2)-adrenergic agonist) into the AV3V region significantly reduced ANG-II-induced water intake. Their injection also induced a significant in crease in plasma ANP concentration and in ANP content in the olfactory bulb (OB), AV3V, medial basal hypothalamus (MBH) and median eminence (ME). Thes e results suggest that the inhibitory effect of both a adrenergic agonists on ANG-IT-induced water intake can be explained, at least in part, by the i ncrease in ANP content and presumed release from these neural structures. T he increased release of ANP from the axons of neurons terminating on the ef fector neurons of the drinking response by stimulation of ANP receptors wou ld inhibit the stimulatory response evoked by the action of ANG-II on its r eceptors on these same effector neurons. (C) 2001 Elsevier Science B.V. All rights reserved.