Barbosa S P, de Gobbi J I, Zilioli L, Camargo L A, Saad W A, Renzi A, de Luca Júnior L A, Menani J V
Department of physiology, School of Dentistry, Paulista State University, UNESP, Araraquara, Brazil.
Brain Res Bull. 1995;37(5):463-6. doi: 10.1016/0361-9230(95)00025-a.
In the present study, we investigated the effect of previous injection of either prazosin (alpha 1-adrenergic antagonist) or atropine (muscarinic cholinergic antagonist) into the medial septal area (MSA) on the pressor and dipsogenic response induced by intracerebroventricular (ICV) injection of carbachol (cholinergic agonist) and angiotensin II (ANGII) in rats. The pressor and dipsogenic responses to ICV carbachol (7 nmol) were reduced after previous treatment of the MSA with atropine (0.5 to 5 nmol), but not prazosin (20 and 40 nmol). The dipsogenic response to ICA ANGII (25 ng) was reduced after prazosin (40 nmol) into the MSA. The pressor response to ICV ANGII was not changed either by previous treatment of the MSA with prazosin or atropine. The present results suggest a dissociation among the pathways subserving the control of dipsogenic and pressor responses to central cholinergic or angiotensinergic activation.
在本研究中,我们调查了先前向大鼠内侧隔区(MSA)注射哌唑嗪(α1肾上腺素能拮抗剂)或阿托品(毒蕈碱胆碱能拮抗剂)对脑室内(ICV)注射卡巴胆碱(胆碱能激动剂)和血管紧张素II(ANGII)所诱导的升压反应和饮水反应的影响。在用阿托品(0.5至5 nmol)而非哌唑嗪(20和40 nmol)预先处理MSA后,对ICV卡巴胆碱(7 nmol)的升压反应和饮水反应降低。向MSA注射哌唑嗪(40 nmol)后,对ICA ANGII(25 ng)的饮水反应降低。用哌唑嗪或阿托品预先处理MSA,对ICV ANGII的升压反应均未改变。目前的结果表明,在介导对中枢胆碱能或血管紧张素能激活的饮水反应和升压反应控制的通路之间存在分离。