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.
D000698:Analgesia; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000503:physiopathology*; D003907:Dexamethasone / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D010146:Pain / Q000503:physiopathology; D010870:Pineal Gland / Q000187:drug effects; D010902:Pituitary Gland / Q000187:drug effects; D051381:Rats; D012083:Renin / Q000494:pharmacology; D012084:Renin-Angiotensin System / Q000187:drug effects; D012149:Restraint, Physical; D012504:Saralasin / Q000494:pharmacology; D012684:Sensory Thresholds / Q000187:drug effects / Q000502:physiology; D013315:Stress, Psychological / Q000503:physiopathology*
D000804:Angiotensin II; D009270:Naloxone; D003907:Dexamethasone; D012083:Renin; D012504:Saralasin