• Physiology & behavior · Aug 1997

    Ventromedial hypothalamus lesions increase the dipsogenic responses and reduce the pressor responses to median preoptic area activation.

    • R Bastos, J V Menani, W A Saad, A Renzi, J E Silveira, and L A Camargo.
    • Department of Physiology, School of Dentistry, Paulista State University (UNESP), Araraquara, SP, Brazil.
    • Physiol. Behav. 1997 Aug 1; 62 (2): 311-6.

    AbstractIn 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 pressor responses. Male rats with sham or electrolytic VMH lesions and a stainless steel cannula implanted into the MnPO were used. Noradrenaline, clonidine (an alpha2-adrenergic receptor agonist), or phenylephrine (an alpha1-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 pressor response induced by ANG II injected into the MnPO was reduced in VMH-lesioned rats, whereas the pressor response induced by clonidine was abolished. Previous treatment with noradrenaline and phenylephrine into the MnPO of sham-lesioned rats produced a pressor 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 pressor responses induced by adrenergic and angiotensinergic activation of the MnPO in rats.

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