Hăulică I, Neamţu C, Stratone A, Petrescu G, Roşca V, Nacu C, Slătineanu S
Physiologie. 1985 Jul-Sep;22(3):165-73.
Studies concerning the variations of the central renin-angiotensin system (RAS) during the immobilization stress in rats have shown a significant increase of the renin-like activity in the hypothalamus and the fronto-parietal cortex together with a manifest decrease in hypophysis and pineal gland. The resulted stress, analgesia, is blocked by the previous administration of naloxone and saralasin. The intracerebral administration of renin and angiotensin II increases the latency time to thermoalgesic stimuli which is reduced, as in the immobilisation stress, by naloxone and saralasin. The chemical hypophysectomy obtained by chronic treatment with dexamethasone, also inhibits the stress-induced analgesia. Epiphysectomy reduces all the same the analgesic effects of the immobilisation stress. The obtained experimental data argue in favour of the participation of the cerebral RAS in stress analgesia through the indirect mechanism of release of opioid peptides.
关于大鼠制动应激期间中枢肾素-血管紧张素系统（RAS）变化的研究表明，下丘脑和额顶叶皮质中的肾素样活性显著增加，同时垂体和松果体明显减少。由此产生的应激镇痛作用可被预先给予的纳洛酮和沙拉新阻断。脑内注射肾素和血管紧张素II可增加对热痛刺激的潜伏期，与制动应激时一样，纳洛酮和沙拉新可缩短该潜伏期。用地塞米松长期治疗所致的化学性垂体切除也可抑制应激诱导的镇痛作用。松果体切除同样可降低制动应激的镇痛效果。所获得的实验数据支持脑RAS通过阿片肽释放的间接机制参与应激镇痛。
