一氧化氮在大鼠臂旁核的降压作用及其机制分析

实验在63只乌拉坦麻醉、琥珀酰胆碱制动、人工呼吸的大鼠上进行。结果如下臂旁核（NPB）内微量注射NO前体L-精氨酸（L-Arg），引起平均动脉压（MAP）显著下降，但对心率无明显影响。NPB内微量注射NO合酶抑制剂N-硝基-L-精氨酸(L-NNA)，引起MAP显著升高。L-Arg在NPB的降压效应可被NPB内预注射L-NNA或鸟苷酸环化酶抑制剂亚甲蓝所阻断。NPB内预注射γ-氨基丁酸（GABA）受体阻断剂荷包牡丹碱，可使L-Arg在NPB的降压效应显著减弱或消失。结果表明①NO在NPB具有降压作用，此作用是通过激活鸟苷酸环化酶而实现的；②NPB的内源性NO具有紧张性降压作用，并参与正常血压水平的维持；③NO在NPB的降压作用至少部分是由该局部的GABA受体介导。

Depressor Effect of NO in Rat Parabrachial Nuclei and Its Mechanisms

The Experiments were performed on 63 urethane anesthetized, suxamethonium chloride paralyzed and artificially ventilated rats. The results were as follows: microinjection of L-Arg, NO precursor, into parabrachial nuclei (NPB) resulted in a marked decrease in the mean arterial pressure (MAP), but the heart rate had no significant change. Microinjection of N-nitro-L-arginine (L-NNA), NO synthase inhibitor, into NPB caused a significant increase in MAP. Preinjection of L-NNA and methylene blue into NPB separately blocked the depressor effect elicited by L-Arg. Preinjection of bicuculine, γ-aminobutyric acid (GABA) receptor antagonist, into NPB significantly reduced or abolished the depressor effect elicited by L-Arg. The above results indicated that: (1) NO has depressor effect in NPB by activating guanylate cyclase; (2) Endogenous NO in NPB has tonic depressor effect and takes part in maintenance of normal blood pressure level; (3) The depressor effect evoked by NO in NPB is at least partly mediated by local GABA receptor.