Evidence of the involvement of cerebral renin-angiotensin in stress analgesia.

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.

Possible opioid participation in the analgesic effects of the renin-angiotensin system.

Using the tail-flick method in 45 rats with a chronic cannula stereotaxically implanted in the third ventricle, a rapid onset, dose related and short lasting analgesia was obtained after intracerebroventricular injection of Ang II 10-15 ng/kg or renin 0.03-0.1 U. Analgesic effects of the endogenous and exogenous Ang II are prevented by naloxone--1 mg/kg i.p. The inhibition of serotonin synthesis with PCPA--400 mg/kg/day i.p. for five days as well as the serotonin-receptor block with ketanserin 0.1 mg/kg i.p. partially prevent analgesic effects of Ang II and renin intracerebral administration. The increase of the pain perception threshold after infusing into the brain Ang II or renin points out a new functional consequence of the possible opioid participation in the central effects of renin-angiotensin system.