Saad W A, Guarda I F, Ferreira A C, de Arruda Camargo L A, Neto A F, dos Santos T A
Department of Physiology and Pathology, School of Dentistry, Paulista State University, Araraquara, Brazil.
Brain Res Bull. 2000 Aug;52(6):491-7. doi: 10.1016/s0361-9230(00)00285-9.
The circumventricular structures and the lateral hypothalamus (LH) have been shown to be important for the central action of angiotensin II (ANGII) on water and electrolyte regulation. Several anatomical findings have demonstrated neural connection between circumventricular structures and the LH. The present experiments were conducted to investigate the role of the alpha-adrenergic antagonists and agonistic injected into the LH on the water intake, sodium and potassium excretion elicited by injections of ANGII into the lateral ventricle (LV). The water intake was measured every 30 min over a period of 120 min. The sodium, potassium and urinary volume were measured over a period of 120 min in water-loaded rats. The injection of ANGII into the LV increased the water intake, which was reduced by previous injection of clonidine (an alpha-2-adrenergic agonist) into the LH. The injection of yohimbine (an alpha-2-adrenergic antagonist) and prazosin (an alpha-1-adrenergic antagonist) into the LH, which was done before injecting ANGII into the LV, also reduced the water intake induced by ANGII. The injection of ANGII into the LV reduced the sodium, potassium and urinary volume. Previous treatment with clonidine attenuated the action of ANGII in reducing the sodium, potassium and urinary volume, whereas previous treatment with yohimbine attenuated the effects of ANGII but with less intensity than that caused by clonidine. Previous treatment with prazosin increased the inhibitory effects of ANGII in those parameters. The injection of yohimbine and prazosin, which was done before the injection of clonidine, attenuated the effect of clonidine on the ANGII mechanism. The results of this study led us to postulate that when alpha-2-adrenergic receptors are blocked, the clonidine may act on the imidazoline receptors to produce its effects on the ANGII mechanism. We may also conclude that the LH is involved with circumventricular structures, which present excitatory and inhibitory mechanisms. Such mechanisms are responsible for regulating the renal excretion of sodium, potassium and water.
室周结构和下丘脑外侧区(LH)已被证明对于血管紧张素II(ANGII)在水和电解质调节方面的中枢作用很重要。多项解剖学研究结果表明室周结构与LH之间存在神经连接。本实验旨在研究向LH内注射α-肾上腺素能拮抗剂和激动剂对向侧脑室(LV)注射ANGII所引起的水摄入、钠和钾排泄的作用。在120分钟内每隔30分钟测量一次水摄入量。在水负荷大鼠中,在120分钟内测量钠、钾和尿量。向LV注射ANGII会增加水摄入量,而先前向LH注射可乐定(一种α-2-肾上腺素能激动剂)可减少这种水摄入量。在向LV注射ANGII之前向LH注射育亨宾(一种α-2-肾上腺素能拮抗剂)和哌唑嗪(一种α-1-肾上腺素能拮抗剂),也可减少ANGII诱导的水摄入量。向LV注射ANGII会减少钠、钾和尿量。先前用可乐定处理可减弱ANGII在减少钠、钾和尿量方面的作用,而先前用育亨宾处理可减弱ANGII的作用,但强度小于可乐定所引起的强度。先前用哌唑嗪处理会增强ANGII在这些参数上的抑制作用。在注射可乐定之前注射育亨宾和哌唑嗪,可减弱可乐定对ANGII机制的作用。本研究结果使我们推测,当α-2-肾上腺素能受体被阻断时,可乐定可能作用于咪唑啉受体以对ANGII机制产生影响。我们还可以得出结论,LH与室周结构有关,后者存在兴奋和抑制机制。这些机制负责调节肾脏对钠、钾和水的排泄。