BLOCKADE OF CENTRAL ANGIOTENSIN-II TYPE-1 AND TYPE-2 RECEPTORS SUPPRESSES ADRENALECTOMY-INDUCED NACL INTAKE IN RATS

Removal of the adrenal glands, the main site for the synthesis of aldo sterone, produces an intake of sodium that is essential for survival. Using central blockade of angiotensin II (Ang II) receptors with Sarll e Ang II, previous studies have shown that this intake depends on the stimulation of the brain angiotensin system. In the present study, usi ng intracerebroventricular injection of specific antagonists of Ang II type 1 (AT1) or type 2 (AT2) receptors (losartan and PD 123319, respe ctively), we confirm that activation of brain angiotensin is essential for the expression of adrenalectomy-induced NaCl intake. Moreover, we show that (a) AT1 but not AT2 receptor blockade alone suppresses NaCl intake and (b) doses of AT1 and AT2 receptor antagonists that separat ely have no effect on NaCl intake, suppress the behavior when combined . It is proposed that AT1 receptors mediate the natriorexigenic effect of Ang II and that AT2 receptors have a permissive role on AT1 recept or stimulation.