McCall R B, Harris L T, King K A
Cardiovascular Disease Research, Upjohn Company, Kalamazoo, MI 49001.
Eur J Pharmacol. 1991 Jun 25;199(2):263-5. doi: 10.1016/0014-2999(91)90468-6.
The present study determined the mechanism by which yohimbine inhibits sympathetic nerve activity in the anesthetized cat. Low i.v. doses of yohimbine increased inferior cardiac nerve discharge as a result of the alpha 2-adrenoceptor antagonist properties of the drug. Higher doses of yohimbine (0.8-1.6 mg/kg) inhibited sympathetic nerve discharge. The inhibition of nerve activity was reversed by i.v. administration of the 5HT1A receptor antagonist spiperone. Similarly we have previously observed spiperone reversal of the sympatholytic effects of the 5-HT1A agonist 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin) but failed to affect nerve activity when given alone. Spiperone failed to reverse the sympatholytic effect of clonidine. These data indicate that high doses of yohimbine inhibit sympathetic nerve activity via a 5HT1A agonist action.
本研究确定了育亨宾抑制麻醉猫交感神经活动的机制。静脉注射低剂量育亨宾会由于该药物的α2-肾上腺素能受体拮抗剂特性而增加心下神经放电。更高剂量的育亨宾（0.8 - 1.6毫克/千克）会抑制交感神经放电。静脉注射5HT1A受体拮抗剂螺哌隆可逆转神经活动的抑制。同样，我们之前观察到螺哌隆可逆转5-HT1A激动剂8-OH-DPAT（8-羟基-2-（二正丙基氨基）四氢萘）的交感神经抑制作用，但单独给药时对神经活动没有影响。螺哌隆未能逆转可乐定的交感神经抑制作用。这些数据表明，高剂量育亨宾通过5HT1A激动剂作用抑制交感神经活动。
