do Vale C F, Camargo G M, Saad W A, Menani J V, Renzi A, Luiz A C, Cerri P S, Camargo L A
Department of Physiology, School of Dentistry, Paulista State University, UNESP, Araraquara, Brazil.
J Auton Nerv Syst. 1997 Sep 10;66(1-2):19-25. doi: 10.1016/s0165-1838(97)00038-6.
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.
在本研究中，我们调查了用鹅膏蕈氨酸造成腹内侧下丘脑（VMH）损伤对正中视前核（MnPO）联合血管紧张素II（ANG II）及肾上腺素能激动剂（去氧肾上腺素、去甲肾上腺素、异丙肾上腺素和可乐定）治疗所诱导的水和钠摄入以及升压反应的影响。使用了植入了MnPO不锈钢套管且接受双侧假手术（载体）或用鹅膏蕈氨酸造成VMH损伤的雄性霍尔兹曼大鼠。在单独的几组中，用利尿剂速尿（20毫克/大鼠）使大鼠缺钠，然后测定水和钠的摄入量以及平均动脉压（MAP）。向假手术损伤大鼠的MnPO注射ANG II（10皮摩尔）可诱导水和钠摄入以及升压反应。VMH损伤减少了ANG II诱导的水摄入并增加了盐水摄入。在假手术大鼠中，向MnPO注射去氧肾上腺素（80纳摩尔）会增加ANG II诱导的水摄入，而去甲肾上腺素（80纳摩尔）和可乐定（40纳摩尔）则会减少ANG II诱导的水摄入，只有向MnPO注射可乐定才会减少钠摄入。在VMH损伤大鼠中，去氧肾上腺素减少了ANG II诱导的水摄入，去甲肾上腺素增加了该水摄入，而可乐定则对ANG II诱导的水摄入无影响。在损伤大鼠中，去氧肾上腺素和去甲肾上腺素减少了ANG II诱导的钠摄入，而可乐定则无变化。VMH损伤大鼠中ANG II诱导的升压反应降低，但VMH损伤大鼠中ANG II与去氧肾上腺素或去甲肾上腺素联合诱导的升压反应比假手术大鼠更大。这些结果表明，VMH对于MnPO的血管紧张素能和肾上腺素能激活所诱导的水和钠摄入变化以及心血管反应很重要。
