Evidence for the involvement of cerebral renin-angiotensin system (RAS) in stress analgesia.
Studies concerning variations of the central renin-angiotensin system (RAS) during immobilization stress in rats have shown a significant increase in renin-like activity in the hypothalamus and fronto-parietal cortex, together with a definite decrease in the hypophysis and pineal gland. The resultant stress analgesia is blocked by the previous administration of naloxone and saralasin (angiotensin II antagonist). The intracerebral administration of renin and angiotensin II produces an increase in latencies to thermoalgesic stimuli; this is reduced, as is immobilization stress, by naloxone and saralasin. Both chemical hypophysectomy obtained by dexamethasone pretreatment as well as surgical epiphysectomy block the stress-induced analgesia. The experimental data obtained 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 / Q000378:metabolism*; D003907:Dexamethasone / Q000494:pharmacology; D007017:Hypophysectomy, Chemical; D007103:Immobilization; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D009619:Nociceptors / Q000187:drug effects; D010870:Pineal Gland / Q000378:metabolism; D010902:Pituitary Gland / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012083:Renin / Q000494:pharmacology; D012084:Renin-Angiotensin System / Q000187:drug effects; D012504:Saralasin / Q000494:pharmacology; D013312:Stress, Physiological / Q000378:metabolism*
D000804:Angiotensin II; D009270:Naloxone; D003907:Dexamethasone; D012083:Renin; D012504:Saralasin