Role of prostaglandins in the aldosterone response to ACTH in sodium depleted human subjects.
It is well established that the response of plasma aldosterone to ACTH is enhanced in the sodium depleted state. The mechanisms for this phenomenon are not clear, however, and the present study was undertaken to determine the possible participation of endogenous prostaglandins. ACTH, 250 ug by i.m. administration, was given to 10 human subjects pretreated in four different ways: 1. Control, receiving a 200 mEq per day sodium diet; 2. Sodium depletion (60 mEq/day sodium plus furosemide) plus indomethacin; 3. Sodium depletion plus indomethacin plus captopril; and 4. Sodium depletion plus captopril. Only in the last group, in which the prostaglandin cyclooxygenase inhibitor, indomethacin, was not given during the sodium depletion, did an exaggerated aldosterone response to ACTH occur (an increase of 468% compared with an increase of 182% during control, P less than 0.005). The angiotensin converting enzyme inhibitor, captopril, did not effect this response. Thus, endogenous prostaglandins appear to be of far greater importance than the renin-angiotensin system in mediating the increased aldosterone response to ACTH administration during the sodium depleted state in man.
D000324:Adrenocorticotropic Hormone; D000450:Aldosterone / Q000097:blood*; D002216:Captopril; D004039:Diet, Sodium-Restricted; D005665:Furosemide; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007213:Indomethacin; D007700:Kinetics; D008297:Male; D011453:Prostaglandins / Q000378:metabolism*; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism*
D011453:Prostaglandins; D000450:Aldosterone; D005665:Furosemide; D000324:Adrenocorticotropic Hormone; D002216:Captopril; D012964:Sodium; D012083:Renin; D006854:Hydrocortisone; D007213:Indomethacin