Van de Kar L D, Urban J H, Lorens S A, Richardson K D
Life Sci. 1985 Mar 25;36(12):1149-55. doi: 10.1016/0024-3205(85)90231-0.
The non benzodiazepine drug, buspirone, produces a dose-dependent biphasic effect on plasma renin activity in non-stressed rats. Low doses (0.1 - 2.0 mg/kg i.p.) decrease while high doses (10.0 - 50.0 mg/kg i.p.) increase plasma renin activity. The maximal decrease in plasma renin activity produced by buspirone (1.0 mg/kg i.p.) was observed 30 minutes post-injection. In addition, buspirone (0.5 and 2.0 mg/kg i.p.) blocked the stress-induced rise in plasma renin activity. This effect of buspirone is in contrast to the previously observed failure of the benzodiazepine anxiolytics to alter the effect of stress on plasma renin activity. Administration of buspirone (0.5 mg/kg i.p.) produced a sustained reduction (15%) in heart rate but did not affect mean arterial pressure. The present data support the view that the mechanism of the anxiolytic action of buspirone is different from that of the benzodiazepines.
非苯二氮䓬类药物丁螺环酮对非应激大鼠的血浆肾素活性产生剂量依赖性双相效应。低剂量(腹腔注射0.1 - 2.0毫克/千克)会降低血浆肾素活性,而高剂量(腹腔注射10.0 - 50.0毫克/千克)则会增加血浆肾素活性。丁螺环酮(腹腔注射1.0毫克/千克)引起的血浆肾素活性最大降幅在注射后30分钟观察到。此外,丁螺环酮(腹腔注射0.5和2.0毫克/千克)可阻断应激诱导的血浆肾素活性升高。丁螺环酮的这种作用与先前观察到的苯二氮䓬类抗焦虑药未能改变应激对血浆肾素活性的影响形成对比。腹腔注射丁螺环酮(0.5毫克/千克)可使心率持续降低(15%),但不影响平均动脉压。目前的数据支持丁螺环酮抗焦虑作用机制与苯二氮䓬类药物不同的观点。