title: Ibotenate lesion of the medial hypothalamus alters the salt intake and pressor responses to activation of the median preoptic nucleus in rats.
abstract: We investigated the influence of ibotenic acid lesions of the medial hypothalamus (MH) on salt appetite and arterial blood pressure responses 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. Previous injection of clonidine and isoproterenol increased, whereas phenylephrine abolished the salt intake induced by ANG II into the MnPO of MH-lesioned rats. Previous injection of norepinephrine and clonidine into the MnPO of sham MH-lesioned rats caused no change in the mean arterial pressure (MAP) induced by ANG II. Under the same conditions, previous injection of phenylephrine increased, whereas isoproterenol reversed the increase in MAP induced by angiotensin II (ANG II). ANG II injected into the MnPO of MH-lesioned rats induce a decrease in MAP compared with sham-lesioned rats. Previous injection of phenylephrine or norepinephrine 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 rats. These data show that ibotenic acid lesion of the MH increases the sodium intake and pressor responses induced by the concomitant angiotensinergic, alpha 2 and beta adrenergic activation of the MnPO, whereas alpha 1 activation may have opposite effects. MH involvement in excitatory and inhibitory mechanisms related to sodium intake and MAP control is suggested.
authors.affiliation: Department of Physiology, School of Dentistry, Paulista State University, UNESP, Araraquara, SP, Brazil.
authors.forename: C F
authors.initials: CF
authors.lastname: do Vale
authors.forename: G M
authors.initials: GM
authors.lastname: Camargo
authors.forename: A
authors.initials: A
authors.lastname: Renzi
authors.forename: A C
authors.initials: AC
authors.lastname: Luiz
authors.forename: W A
authors.initials: WA
authors.lastname: Saad
authors.forename: S
authors.initials: S
authors.lastname: Hetem
authors.forename: L A
authors.initials: LA
authors.lastname: Camargo
mesh_terms: D000322:Adrenergic Agonists / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D004435:Eating / Q000502:physiology*; D018690:Excitatory Amino Acid Agonists / Q000008:administration & dosage / Q000633:toxicity*; D007033:Hypothalamus, Middle / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D007051:Ibotenic Acid / Q000008:administration & dosage / Q000633:toxicity*; D007267:Injections; D008297:Male; D011301:Preoptic Area / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D012982:Sodium, Dietary
chemical_list: D000322:Adrenergic Agonists; D018690:Excitatory Amino Acid Agonists; D012982:Sodium, Dietary; D000804:Angiotensin II; D007051:Ibotenic Acid