Szemeredi K, Zukowska-Grojec Z, Bagdy G, Hill J, Kopin I J
National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Eur J Pharmacol. 1988 Jan 19;145(3):251-5. doi: 10.1016/0014-2999(88)90426-8.
To study the in vivo peripheral effects of clonidine on sympathetic neuronal function we measured, after different doses of clonidine, plasma norepinephrine (NE) and blood pressure (BP) responses during electric stimulation of sympathetic outflow in pithed male Sprague-Dawley rats. In this preparation, clonidine produced dose-dependent inhibition of the sympathetic stimulation-induced pressor and plasma NE responses. The dose of clonidine inhibiting the NE response by 50% (ID50) was 14.2 +/- 0.3 micrograms/kg i.v., while ID50 for the diastolic pressor response was 22.0 +/- 0.2 micrograms/kg i.v. Since clonidine did not alter the relationship between NE released into the plasma and the pressor responses, the entire effect of clonidine in decreasing the pressor response to sympathetic stimulation may be attributed to its presynaptic alpha 2-adrenoceptor-mediated inhibition of NE release.
为研究可乐定对交感神经元功能的体内外周效应，我们在雄性斯普拉格 - 道利大鼠脊髓横断后，给予不同剂量的可乐定，然后测量电刺激交感神经传出时血浆去甲肾上腺素（NE）和血压（BP）的反应。在此实验准备中，可乐定对交感神经刺激诱发的升压反应和血浆NE反应产生剂量依赖性抑制。使NE反应抑制50%（半数抑制剂量，ID50）的可乐定静脉注射剂量为14.2±0.3微克/千克，而舒张压升压反应的ID50为22.0±0.2微克/千克。由于可乐定并未改变释放到血浆中的NE与升压反应之间的关系，可乐定降低对交感神经刺激的升压反应的全部效应可能归因于其通过突触前α2 - 肾上腺素能受体介导的对NE释放的抑制作用。
