Bastos, R.Menani, José Vanderlei [UNESP]Saad, W. A.Renzi, Antonio [UNESP]Silveira, JENCamargo, LADA2014-05-202014-05-201997-08-01Physiology & Behavior. Oxford: Pergamon-Elsevier B.V., v. 62, n. 2, p. 311-316, 1997.0031-9384http://hdl.handle.net/11449/35627In this study, we investigated the participation of adrenergic receptors of the median preoptic area (MnPO) and the participation of ventromedial hypothalamus (VMH) in angiotensin II- (ANG II)-induced water intake and presser responses. Male rats with sham or electrolytic VMH lesions and a stainless steel cannula implanted into the MnPO were used. Noradrenaline, clonidine (an alpha(2)-adrenergic receptor agonist), or phenylephrine (an alpha(1)-adrenergic receptor agonist) injected into the MnPO of sham-lesioned rats reduced water ingestion induced by ANG II injected into the same area. In VMH-lesioned rats ANG II-induced water intake increased with a previous injection of noradrenaline, phenylephrine, or isoproterenol. The presser response induced by ANG II injected into the MnPO was reduced in VMH-lesioned rats, whereas the presser response induced by clonidine was abolished. Previous treatment with noradrenaline and phenylephrine into the MnPO of sham-lesioned rats produced a presser response, and a hypotensive response was obtained with the previous administration of noradrenaline, phenylephrine or isoproterenol into the MnPO of VMH-lesioned rats. These results show that VMH is essential for the dipsogenic and presser responses induced by adrenergic and angiotensinergic activation of the MnPO in rats. (C) 1997 Elsevier B.V.311-316engwater intakearterial pressureANG IIadrenergic agonistsMnPOVMHArtigo10.1016/S0031-9384(97)88986-XWOS:A1997XN41000013Acesso restrito10235978701181056551236936295697