大鼠延髓A5区降压、降心率效应的机制及其与A1区之比较

在与上一篇论文(关于A_1区)相同的条件下,(1) 用谷氨酸钠兴奋大鼠A_5区,和A_1区类似,也产生明显的降压、降心率效应。(2) 切断双侧颈迷走神经也明显衰减兴奋A_5区的心血管作用。(3) 将不同受体阻断剂注入延髓头端腹外侧区对兴奋A_5区引起的降压,降心率反应之影响,与A_1区比较有所不同:酚妥拉明、心得安、纳洛酮和荷包牡丹碱均能明显衰减A_5区的降压、降心率效应(心得安和荷包牡丹碱甚至反转之),表明除α-,β-,GABA受体之外,阿片受体也中介A_5区的降压降心率作用。

MECHANISMS UNDERLYING DEPRESSOR AND BRADYCARDIA EFFECTS OF A_5-EXCITATION (COMPARED WITH THAT OF A_1-EXCITATION) IN RATS

Experiments were performed under the same condition described in the accompanying paper. (1) Injection of sodium L-glutamate (Glu) into A5 area of rat induced depressor and bradycardia responses, as Glu-injection into A1 area did. (2) Bilateral vagotomy also markedly attenuated the cardiovascular effect of Glu-injection into A5. (3) Influences of the receptor blockers injected into rostral ventrolateral medulla (RVL) on the depressor and bradycardia responses of Glu-injection into A5 were slightly different from those of the same receptor blockers administered into RVL: phentolamine, propranolol, naloxone and bicuculline all markedly reduced the depressor and bradycardia effects of A5-excitation (propranolol and bicuculline even reversed these effects). These results indicate that not only alpha-, beta-, GABA receptors, but also opiate receptors mediate the depressor and bradycardia effects of A5.