Adrenal involvement in captopril-induced potentiation of morphine analgesia.
The involvement of the angiotensin-adrenal system as a possible mechanism in the potentiation of morphine analgesia by the angiotensin-converting enzyme inhibitor, captopril (SQ 14225), was studied in rats. Captopril pretreatment sensitized the animals to the analgesic effects of morphine while angiotensin II exerted an attenuating influence. These effects, however, were not demonstrable in adrenalectomized animals. Although captopril could inhibit the plasma angiotensin-converting enzyme activity, it appeared to have no significant effect on the brain enzyme. It has been suggested that the effects of captopril and angiotensin II on morphine analgesia are mediated indirectly through their effects on adrenal function.
D000311:Adrenal Glands / Q000502:physiology*; D000698:Analgesia; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D004357:Drug Synergism; D008297:Male; D008901:Mineralocorticoids; D009020:Morphine / Q000494:pharmacology*; D007703:Peptidyl-Dipeptidase A / Q000032:analysis; D011392:Proline / Q000031:analogs & derivatives*; D051381:Rats; D011919:Rats, Inbred Strains
D008901:Mineralocorticoids; D000804:Angiotensin II; D009020:Morphine; D011392:Proline; D002216:Captopril; D007703:Peptidyl-Dipeptidase A