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.
The presence and distribution of renin-like activity in hypophysis, pineal gland and some neural tissues were studies in both normal and salt-loaded rats. The Boucher micromethod was used to detect enzymatic activity. In normal rats both the pituitary and pineal glands contained significantly higher values of renin-like activity than did the other tissues examined. In salt-loaded animals there was a significant decrease of the renin-like activity of the glandular tissue while in the other brain areas the activity increased. The results are discussed in terms of the possible physiological role of the central renin-angiotensin system in the regulation of fluid and electrolyte balance.
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