title: Effect of ibotenate lesions of the ventromedial hypothalamus on the water and salt intake induced by activation of the median preoptic nucleus in sodium-depleted rats.
abstract: In this study we investigated the influence of a ventromedial hypothalamus (VMH) lesion with ibotenic acid on water and sodium intake and pressor responses induced by combined treatment of the median preoptic nucleus (MnPO) with angiotensin II (ANG II) and adrenergic agonists (phenylephrine, norepinephrine, isoproterenol and clonidine). Male Holtzman rats with a stainless steel cannula implanted into the MnPO and bilateral sham (vehicle) or VMH lesions with ibotenic acid were used. The ingestion of water and sodium and mean arterial pressure (MAP) were determined in separate groups submitted to sodium depletion with the diuretic furosemide (20 mg/rat). ANG II (10 pmol) injection into the MnPO of sham-lesioned rats induced water and sodium intake and pressor responses. VMH-lesion reduced ANG II-induced water intake and increased saline intake. In sham rats phenylephrine (80 nmol) into MnPO increased, whereas norepinephrine (80 nmol) and clonidine (40 nmol) reduced ANG II-induced water intake while sodium intake was reduced only by clonidine into MnPO. In VMH-lesioned rats, phenylephrine reduced, noradrenaline increased and clonidine produced no effect on ANG II-induced water intake. In lesioned rats ANG II-induced sodium intake was reduced by phenylephrine and noradrenaline, whereas clonidine produced no change. ANG II-induced pressor response was reduced in VMH-lesioned rats, but the pressor response combining ANG II and phenylephrine or noradrenaline in VMH-lesioned rats was bigger than sham rats. These results show that the VMH is important for the changes in water and sodium intake and cardiovascular responses induced by angiotensinergic and adrenergic activation of the MnPO.
authors.affiliation: Department of Physiology, School of Dentistry, Paulista State University, UNESP, Araraquara, Brazil.
authors.forename: C F
authors.initials: CF
authors.lastname: do Vale
authors.forename: G M
authors.initials: GM
authors.lastname: Camargo
authors.forename: W A
authors.initials: WA
authors.lastname: Saad
authors.forename: J V
authors.initials: JV
authors.lastname: Menani
authors.forename: A
authors.initials: A
authors.lastname: Renzi
authors.forename: A C
authors.initials: AC
authors.lastname: Luiz
authors.forename: P S
authors.initials: PS
authors.lastname: Cerri
authors.forename: L A
authors.initials: LA
authors.lastname: Camargo
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000804:Angiotensin II / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004326:Drinking / Q000187:drug effects*; D004435:Eating / Q000187:drug effects*; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity*; D007051:Ibotenic Acid / Q000633:toxicity*; D008297:Male; D008845:Microinjections; D011301:Preoptic Area / Q000502:physiology*; D051381:Rats; D012964:Sodium / Q000172:deficiency / Q000502:physiology*; D017673:Sodium Chloride, Dietary; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology; D014697:Ventromedial Hypothalamic Nucleus / Q000502:physiology*
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D018690:Excitatory Amino Acid Agonists; D017673:Sodium Chloride, Dietary; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D007051:Ibotenic Acid; D012964:Sodium