Nurminen M L, Culman J, Haass M, Chung O, Unger T
Institute of Biomedicine, Department of Pharmacology and Toxicology, University of Helsinki, Finland.
Eur J Pharmacol. 1998 Nov 27;362(1):61-7. doi: 10.1016/s0014-2999(98)00726-2.
The effects of moxonidine on blood pressure, heart rate and sympathetic tone were studied in conscious spontaneously hypertensive rats. Intravenous moxonidine (80 nmol) transiently increased blood pressure without affecting heart rate or splanchnic nerve activity. Moxonidine (20-80 nmol) given into the fourth cerebral ventricle dose-dependently lowered mean arterial pressure, heart rate and sympathetic outflow (maximally by 60 +/- 3 mm Hg, 148 +/- 10 beats min(-1) and 15 +/- 3 microV). Moxonidine was more effective by this route than after the injection into the lateral ventricle. Clonidine (20-80 nmol) produced an initial pressor response after both intracerebroventricular routes of administration. A decrease in blood pressure was observed only when clonidine was given into the fourth ventricle. Clonidine decreased heart rate and splanchnic nerve activity similarly like moxonidine when the substances were given into the fourth ventricle. The data imply that the hypotensive effect of moxonidine is related to central sympathoinhibition. The main site of this action appears to be in the brainstem region.
在清醒的自发性高血压大鼠中研究了莫索尼定对血压、心率和交感神经张力的影响。静脉注射莫索尼定(80 nmol)可使血压短暂升高,而不影响心率或内脏神经活动。向第四脑室注射莫索尼定(20 - 80 nmol)可剂量依赖性地降低平均动脉压、心率和交感神经输出(最大降低60±3 mmHg、148±10次/分钟和15±3 μV)。通过该途径给药时,莫索尼定比注射到侧脑室后更有效。可乐定(20 - 80 nmol)经两种脑室内给药途径给药后均产生初始升压反应。仅当可乐定注入第四脑室时才观察到血压下降。当将这些物质注入第四脑室时,可乐定降低心率和内脏神经活动的情况与莫索尼定类似。这些数据表明,莫索尼定的降压作用与中枢交感神经抑制有关。该作用的主要部位似乎在脑干区域。