Punnen S, Sapru H N
J Cardiovasc Pharmacol. 1986 Sep-Oct;8(5):950-6. doi: 10.1097/00005344-198609000-00011.
Pressor (VLPA) and depressor (VLDA) areas of the ventrolateral medulla were identified by microinjections of L-glutamate in urethane-anesthetized rats. Cardiovascular effects of opiate agonists microinjected into the same sites were then studied. Agents used to stimulate mu, delta, sigma, kappa, and beta-endorphin (epsilon) receptors were morphiceptin, D-Ala2-D-Leu5-enkephalin, N-allyl-normetazocine, dynorphin, and beta-endorphin, respectively. Opiate receptor stimulation in VLPA decreased blood pressure (BP) and heart rate (HR), while in VLDA it increased BP and HR. Thus, it is the site of injection rather than the type of opiate receptor that determines cardiovascular responses. Naloxone, an opiate antagonist, reversed and prevented these responses. Abolition of cardiovascular responses by spinal transection at the C1 level indicated that the sympathetic nervous system mediated these responses. The following mechanism is proposed for these actions of opiates: Cell bodies in VLPA, but not in VLDA, project to the intermediolateral cell column of the spinal cord. Opiates inhibit VLPA and lower BP and HR by decreasing sympathetic outflow. Opiate-induced inhibition of VLDA, which has an inhibitory effect on VLPA, results in an increase in BP and HR.
通过向乌拉坦麻醉的大鼠脑桥腹外侧髓质内微量注射L-谷氨酸来确定其升压区（腹外侧延髓前区，VLPA）和降压区（腹外侧延髓后区，VLDA）。然后研究了向相同部位微量注射阿片类激动剂后的心血管效应。用于刺激μ、δ、σ、κ和β-内啡肽（ε）受体的药物分别是吗啡肽、D-丙氨酸2-D-亮氨酸5-脑啡肽、N-烯丙基去甲唑新、强啡肽和β-内啡肽。在VLPA中刺激阿片受体可降低血压（BP）和心率（HR），而在VLDA中则升高BP和HR。因此，决定心血管反应的是注射部位而非阿片受体类型。阿片拮抗剂纳洛酮可逆转并阻止这些反应。在C1水平进行脊髓横断后心血管反应消失，表明交感神经系统介导了这些反应。针对阿片类药物的这些作用提出了以下机制：VLPA中的细胞体（而非VLDA中的）投射至脊髓的中间外侧细胞柱。阿片类药物通过减少交感神经传出活动来抑制VLPA并降低BP和HR。阿片类药物对VLDA的抑制作用会导致BP和HR升高，而VLDA对VLPA具有抑制作用。
