de Jong W, Petty M A, Sitsen J M
Chest. 1983 Feb;83(2 Suppl):306-8. doi: 10.1378/chest.83.2_supplement.306.
Beta-endorphin and related opioid peptides are neuropeptides which appear to play a role in cardiovascular regulation which is supported by altered nociceptive responsiveness in hypertensive animals. In spontaneously hypertensive rats the pain threshold for electric stimulation is elevated; these rats show increased response latency time in a hot plate test. The opiate antagonist naloxone reverses these values to that of the normotensive controls. In other forms of experimental hypertension, eg, renal hypertension (one-clip, two-kidney model), no change in pain sensitivity is apparent. Sinoaortic baroreceptor denervation causes a labile hypertension without changes in hot plate response. Administration of beta-endorphin into the nucleus of the solitary tract (NTS) gradually decreases blood pressure and heart rate without affecting respiratory frequency. These cardiovascular effects are blocked by naloxone as well as by an antibody to beta-endorphin. In contrast to the effects of beta-endorphin, microinjection of enkephalins into the NTS increases blood pressure and heart rate. The data suggest the existence of two separate endorphin systems at the level of the NTS, one a depressor and another a pressor system. The depressor influence of beta-endorphin may play a role in the mechanism of action of antihypertensive agents such as methyldopa and clonidine. Our data support a role of endorphins as neuropeptides involved in cardiovascular regulation, exerting a dual influence at the level of the NTS.
β-内啡肽及相关阿片肽是神经肽，似乎在心血管调节中发挥作用，这一观点得到了高血压动物伤害性反应改变的支持。在自发性高血压大鼠中，电刺激的痛阈升高；这些大鼠在热板试验中表现出反应潜伏期延长。阿片拮抗剂纳洛酮可使这些数值恢复到正常血压对照组的水平。在其他形式的实验性高血压中，如肾性高血压（单夹双肾模型），疼痛敏感性无明显变化。去窦主动脉压力感受器会导致不稳定的高血压，但热板反应无变化。将β-内啡肽注入孤束核（NTS）会逐渐降低血压和心率，而不影响呼吸频率。这些心血管效应会被纳洛酮以及β-内啡肽抗体阻断。与β-内啡肽的作用相反，将脑啡肽微量注射到NTS中会增加血压和心率。数据表明在NTS水平存在两个独立的内啡肽系统，一个是降压系统，另一个是升压系统。β-内啡肽的降压作用可能在甲基多巴和可乐定等抗高血压药物的作用机制中发挥作用。我们的数据支持内啡肽作为参与心血管调节的神经肽发挥作用，在NTS水平发挥双重影响。
