Gordon F J, Brody M J, Fink G D, Buggy J, Johnson A K
Brain Res. 1979 Dec 7;178(1):161-73. doi: 10.1016/0006-8993(79)90095-7.
The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.
通过用6-羟基多巴胺(6-OHDA)耗竭大鼠中枢神经系统(CNS)中的儿茶酚胺,评估了这些胺类在高血压发展和饮水行为控制中的作用。脑室内注射6-OHDA完全阻止了单肾肾性高血压的发展,并消除了相关的饮水量增加。当用皮下注射血管紧张素II(AII)和高渗氯化钠刺激时,经6-OHDA处理的大鼠表现出饮水行为缺陷。脑室内注射AII和卡巴胆碱产生的急性升压反应实际上被中枢儿茶酚胺耗竭所消除。然而,中枢胆碱能刺激引起的饮水保持完好,而AII引起的饮水则显著减少。这些数据表明,单肾肾性高血压的发展及其伴随的饮水增加需要CNS儿茶酚胺的完整性。此外,破坏含中枢儿茶酚胺的神经元可使中枢胆碱能刺激而非AII刺激产生的升压反应和饮水反应发生特异性分离。