Bastos, R.Saad, W. A.Menani, José Vanderlei [UNESP]Renzi, Antonio [UNESP]Silveira, JENCamargo, LAD2014-05-202014-05-201994-02-04Brain Research. Amsterdam: Elsevier B.V., v. 636, n. 1, p. 81-86, 1994.0006-8993http://hdl.handle.net/11449/37719In this study, we investigated the participation of adrenergic neurotransmission in angiotensin II- (ANGII)-induced water intake and urinary electrolyte excretion by means of injection of the alpha(1)-, alpha(2)-, and beta-adrenoceptor antagonists and ANGII into the medial preoptic area (MPOA) in rats. Prazosin (an alpha(1)-adrenergic antagonist) antagonized the water ingestion, Na+, K+ and urine excretion induced by ANGII, whereas yohimbine (an alpha(2)-adrenergic antagonist) enhanced the Na+, K+ and urine excretion induced by ANGII. Propranolol (a nonselective beta-adrenoceptor blocker) antagonized the water ingestion and enhanced the Na+ and urine excretion induced by ANGII. Previous treatment with prazosin reduced the presser responses to ANGII, whereas yohimbine had opposite effects. Previous injection of propranolol produced no effects in the presser responses to ANGII. These results suggest that the adrenergic neurotransmission in the MPOA may actively participate in ANGII-induced dipsogenesis, natriuresis, kaliuresis and diuresis in a process that involves alpha(1)-, alpha(2)-, and beta-adrenoceptors.81-86engWATER INTAKEFLUID BALANCEELECTROLYTE BALANCEAV3V REGIONADRENERGIC RECEPTORArtigo10.1016/0006-8993(94)90178-3WOS:A1994MV32400010Acesso restrito10235978701181056551236936295697