da Silva R K, Saad W A, Renzi A, Menani J V, Camargo L A
Department of Physiology, School of Dentistry, Paulista State University, Araraquara, SP, Brazil.
J Auton Nerv Syst. 1995 Jun 25;53(2-3):195-204. doi: 10.1016/0165-1838(94)00176-k.
In this study we investigated the influence of electrolytic lesion of the lateral hypothalamus (LH) on the water and salt appetite, and the natriuretic, diuretic and cardiovascular effects induced by angiotensinergic, cholinergic and noradrenergic stimulation of the median preoptic nucleus (MnPO) in rats. Male Holtzman rats were implanted with a cannula into the MnPO. Other groups of sham- and LH-lesioned rats received a stainless steel cannula implanted into the MnPO. ANGII injection into the MnPO induced water and sodium intake, and natriuretic, diuretic, pressor and tachycardic responses. Carbachol induced water intake, and natriuretic, pressor and bradycardic responses, whereas noradrenaline increased urine, sodium excretion and blood pressure, and induced bradycardia. In rats submitted to LH-lesion only, water and sodium intake was reduced compared with sham rats. LH lesion also reduced the sodium ingestion induced by ANGII (12 ng) into the MnPO. In LH-lesioned rats, the dipsogenic, diuretic and pressor responses induced by ANGII (12 ng), carbachol (2 nmol) and noradrenaline (20 nmol) injection into the MnPO were reduced. The same occurred with sodium excretion when carbachol (2 nmol) and noradrenaline (20 nmol) were injected into the MnPO of LH-lesioned rats, whereas ANGII (12 ng) induced an increase in sodium excretion. These data show that electrolytic lesion of the LH reduces fluid and sodium intake, and pressor responses to angiotensinergic, cholinergic and noradrenergic activation of the MnPO. LH involvement with MnPO excitatory and inhibitory mechanisms related to water and sodium intake, sodium excretion and cardiovascular control is suggested.
在本研究中，我们调查了大鼠下丘脑外侧区（LH）电解损伤对水盐食欲的影响，以及正中视前核（MnPO）受血管紧张素能、胆碱能和去甲肾上腺素能刺激后所诱导的利钠、利尿和心血管效应。将雄性霍尔茨曼大鼠的套管植入MnPO。其他假手术组和LH损伤组大鼠则在MnPO植入不锈钢套管。向MnPO注射血管紧张素II（ANGII）可诱导水和钠摄入以及利钠、利尿、升压和心动过速反应。卡巴胆碱可诱导水摄入以及利钠、升压和心动过缓反应，而去甲肾上腺素则增加尿量、钠排泄和血压，并诱导心动过缓。仅接受LH损伤的大鼠与假手术大鼠相比，水和钠摄入量减少。LH损伤还减少了向MnPO注射ANGII（12 ng）所诱导的钠摄入。在LH损伤的大鼠中，向MnPO注射ANGII（12 ng）、卡巴胆碱（2 nmol）和去甲肾上腺素（20 nmol）所诱导的饮水、利尿和升压反应均减弱。当向LH损伤大鼠的MnPO注射卡巴胆碱（2 nmol）和去甲肾上腺素（20 nmol）时，钠排泄情况也是如此，而注射ANGII（12 ng）则会导致钠排泄增加。这些数据表明，LH的电解损伤会减少液体和钠的摄入，以及对MnPO血管紧张素能、胆碱能和去甲肾上腺素能激活的升压反应。提示LH参与了与水钠摄入、钠排泄和心血管控制相关的MnPO兴奋和抑制机制。
