IBOTENATE LESION OF THE MEDIAL HYPOTHALAMUS ALTERS THE SALT INTAKE AND PRESSOR-RESPONSES TO ACTIVATION OF THE MEDIAN PREOPTIC NUCLEUS IN RATS

We investigated the influence of ibotenic acid lesions of the medial h ypothalamus (MH) on salt appetite and arterial blood pressure response s induced by angiotensinergic and adrenergic stimulation of the median preoptic nucleus (MnPO) of rats. Previous injection of the adrenergic agonists norepinephrine, clonidine, phenylephrine, and isoproterenol into the MnPO of sham MH-lesioned rats caused no change in the sodium intake induced by ANG II. ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Previo us injection of clonidine and isoproterenol increased, whereas phenyle phrine abolished the salt intake induced by ANG II into the MnPO of MH -lesioned rats. Previous injection of norepinephrine and clonidine int o the MnPO of sham MH-lesioned rats caused no change in the mean arter ial pressure (MAP) induced by ANG II. Under the same conditions, previ ous injection of phenylephrine increased, whereas isoproterenol revers ed the increase in MAP induced by angiotensin II (ANG II). ANG II inje cted into the MnPO of MH-lesioned rats induce a decrease in MAP compar ed with sham-lesioned rats. Previous injection of phenylephrine or nor epinephrine into the MnPO of MH-lesioned rats induced a negative MAP, whereas pretreatment with clonidine or isoproterenol increased the MAP produced by ANG II injected into the MnPO of sham- or MH-lesioned rat s. These data show that ibotenic acid lesion of the MH increases the s odium intake and presser responses induced by the concomitant angioten sinergic, alpha(2) and beta adrenergic activation of the MnPO, whereas alpha(1) activation may have opposite effects. MH involvement in exci tatory and inhibitory mechanisms related to sodium intake and MAP cont rol is suggested.