Colombari D S, Haibara A S, Camargo L A, Saad W A, Renzi A, DeLuca L A, Menani J V
Department of Physiology, School of Dentistry, Paulista State University, Araraquara, SP, Brazil.
Brain Res Bull. 1994;33(3):249-54. doi: 10.1016/0361-9230(94)90191-0.
In the present study we investigated the effect of electrolytic lesion of the medial septal area (MSA) on the pressor and dipsogenic response to cholinergic activation and angiotensin II (ANGII) injection into the subfornical organ (SFO) in rats. In addition the effect of MSA lesion on the natriuresis, kaliuresis and diuresis after cholinergic activation of the SFO was also investigated. Sham- and MSA-lesioned rats with a stainless steel cannula implanted into the SFO was used. The injection of ANGII (12 ng) into the SFO in sham rats produced pressor (24 +/- 2 mmHg) and dipsogenic (9.6 +/- 1.1 ml/h) responses. MSA lesion, both acute (2-6 days) and chronic (15-19 days), reduced the pressor (14 +/- 2 mmHg) and dipsogenic (2.7 +/- 1 ml/h) responses to ANGII into SFO. The injection of the cholinergic agonist carbachol (2 nmol) into the SFO in sham rats produced pressor (48 +/- 4 mmHg), dipsogenic (10 +/- 1.2 ml/h), natriuretic (457 +/- 58 microEq/2 h) and kaliuretic (249 +/- 16 microEq/2 h) responses. Acute, but not chronic MSA lesion reduced the pressor (27 +/- 3 mmHg), natriuretic (198 +/- 55 microEq/2 h) and kaliuretic (128 +/- 16 microEq/2 h) responses to carbachol into SFO. No change in the dipsogenic response to carbachol into the SFO was observed in MSA-lesioned rats. Antidiuresis after carbachol was observed only in MSA-lesioned rats. The present results show that the MSA plays a role on the pressor, natriuretic and kaliuretic responses to cholinergic activation of the SFO in rats and on the pressor and dipsogenic responses to ANGII into the same area.(ABSTRACT TRUNCATED AT 250 WORDS)
在本研究中,我们调查了内侧隔区(MSA)电解损伤对大鼠穹窿下器(SFO)胆碱能激活和注射血管紧张素II(ANGII)后的升压及饮水反应的影响。此外,还研究了MSA损伤对SFO胆碱能激活后的尿钠排泄、尿钾排泄和利尿的影响。使用了植入SFO不锈钢套管的假手术和MSA损伤大鼠。在假手术大鼠中,向SFO注射ANGII(12 ng)可产生升压反应(24±2 mmHg)和饮水反应(9.6±1.1 ml/h)。急性(2 - 6天)和慢性(15 - 19天)的MSA损伤均降低了对注入SFO的ANGII的升压反应(14±2 mmHg)和饮水反应(2.7±1 ml/h)。在假手术大鼠中,向SFO注射胆碱能激动剂卡巴胆碱(2 nmol)可产生升压反应(48±4 mmHg)、饮水反应(10±1.2 ml/h)、尿钠排泄反应(457±58微当量/2小时)和尿钾排泄反应(249±16微当量/2小时)。急性而非慢性的MSA损伤降低了对注入SFO的卡巴胆碱的升压反应(27±3 mmHg)、尿钠排泄反应(198±55微当量/2小时)和尿钾排泄反应(128±16微当量/2小时)。在MSA损伤大鼠中,未观察到对注入SFO的卡巴胆碱的饮水反应有变化。仅在MSA损伤大鼠中观察到卡巴胆碱后的抗利尿作用。目前的结果表明,MSA在大鼠对SFO胆碱能激活的升压、尿钠排泄和尿钾排泄反应以及对注入同一区域的ANGII的升压和饮水反应中起作用。(摘要截断于250字)