Freiria-Oliveira Andre H, Blanch Graziela T, Camargo Luis A A, Menani José V, Saad Wilson A
Department of Pathology and Physiology, School of Dentistry, São Paulo State University (UNESP), R. Humaitá, 1680, 14801-903, Araraquara, SP, Brazil.
Regul Pept. 2009 Oct 9;157(1-3):14-8. doi: 10.1016/j.regpep.2009.07.002. Epub 2009 Jul 10.
Previous studies have shown that different parts of the septal area may have opposite roles in the control of water intake and cardiovascular responses. In the present study we investigated the effects of electrolytic lesions of the intermediate nucleus of the lateral septal area (LSI) on cardiovascular and dipsogenic responses to intracerebroventricular (icv) angiotensin II (ANG II) and water intake induced by other different stimuli. Male Holtzman rats (280-320 g of body weight, n=6-16/group) with sham or electrolytic lesions of the LSI and a stainless steel cannula implanted into the lateral ventricle (LV) were used. The LSI lesions did not affect body weight or daily water intake. However, LSI lesions reduced water intake and pressor responses induced by icv ANG II (4.10(-2) nmol). The LSI lesions also slightly reduced water intake induced by 24 h of water deprivation or isoproterenol (30 microg/kg) subcutaneously, but did not affect water intake induced by intragastric 2 ml of 2 M NaCl load. The results suggest that LSI is part of the forebrain circuitry activated by ANG II to produce pressor and dipsogenic responses. However, the same nucleus is not involved in the dipsogenic responses to central osmoreceptor activation.
以往的研究表明，隔区的不同部位在控制水摄入和心血管反应方面可能具有相反的作用。在本研究中，我们调查了外侧隔区中间核（LSI）的电解损伤对心血管和饮水反应的影响，这些反应是由脑室内（icv）注射血管紧张素II（ANG II）以及其他不同刺激诱导的饮水行为所引发的。我们使用了雄性霍尔茨曼大鼠（体重280 - 320克，每组n = 6 - 16只），这些大鼠接受了LSI的假手术或电解损伤，并在侧脑室（LV）植入了不锈钢套管。LSI损伤不影响体重或每日水摄入量。然而，LSI损伤降低了由icv注射ANG II（4.10(-2) nmol）诱导的水摄入量和升压反应。LSI损伤还略微降低了由24小时禁水或皮下注射异丙肾上腺素（30微克/千克）诱导的水摄入量，但不影响由胃内注入2毫升2 M NaCl负荷诱导的水摄入量。结果表明，LSI是ANG II激活以产生升压和饮水反应的前脑回路的一部分。然而，同一核团不参与对中枢渗透压感受器激活的饮水反应。
