Shockley D C, Wade L H, Williams-Johnson M M
Department of Pharmacology, Meharry Medical College, Nashville, TN 37208.
Life Sci. 1993;53(3):251-9. doi: 10.1016/0024-3205(93)90676-t.
The alpha-2 adrenoceptor agonists, clonidine, guanabenz, and guanfacine, injected subcutaneously produced a dose-related diuresis. The maximal effect occurred at 2h after administration of clonidine 192 micrograms/kg or 960 micrograms/kg of guanabenz and guanfacine. The alpha-2 antagonist, yohimbine, in doses of 1-8 mg/kg administered prior to the agonists caused a dose-dependent decrease in urine output. The action of the three agonists at alpha-2 adrenoceptors was supported by the observation that the alpha-1 adrenoceptor agonist, prazosin (0.61-2.5 mg/kg), administered prior to each agonist caused an inconsistent decrease in the elevated urinary output caused by clonidine, guanabenz and guanfacine. These results indicate that stimulation of alpha-2 adrenoceptors causes diuresis in the rat.
皮下注射α-2肾上腺素能受体激动剂可乐定、胍那苄和胍法辛可产生剂量相关的利尿作用。给予192微克/千克可乐定或960微克/千克胍那苄和胍法辛后2小时出现最大效应。在给予激动剂之前，以1 - 8毫克/千克的剂量给予α-2拮抗剂育亨宾，可导致尿量呈剂量依赖性减少。α-1肾上腺素能受体激动剂哌唑嗪（0.61 - 2.5毫克/千克）在每种激动剂之前给药，可使可乐定、胍那苄和胍法辛引起的尿量增加出现不一致的减少，这一观察结果支持了这三种激动剂对α-2肾上腺素能受体的作用。这些结果表明，刺激α-2肾上腺素能受体可导致大鼠利尿。
