Role of the renin-angiotensin system in enhancing the aldosterone response to adenocorticotropin during acute sodium depletion in normal subjects.
The role of the renin-angiotensin system in enhancing aldosterone responsiveness to ACTH during acute sodium depletion was studied in 14 healthy medical students. Acute sodium depletion was achieved by oral treatment with 80 mg furosemide and 200 mg SQ 14,225 for 1 day. The im administration of 250 micrograms alpha ACTH-(1-24) or vehicle was performed at 0800-0900 h both on the day after ad libitum diet (control) and 1 h after the oral administration of 50 mg SQ 14,225 on the day after acute sodium depletion. Treatments with furosemide and SQ 14,225 before both ACTH and vehicle administration induced a reproducible sodium depletion, accompanied by a marked increase in PRA and no significant increase in plasma aldosterone. The administration of ACTH, but not of vehicle, produced significant increases in plasma aldosterone in both control and acute sodium-depleted subjects. However, the ACTH-induced increases in plasma aldosterone and their maximal net and percent increments during acute sodium depletion were significantly greater than control values. It is concluded that angiotensin II does not play an important role in enhancing the aldosterone-stimulating activity of ACTH during acute sodium depletion and that sodium depletion per se may be responsible for this enhancement.
D000324:Adrenocorticotropic Hormone; D000328:Adult; D000450:Aldosterone / Q000097:blood*; D000809:Angiotensins / Q000378:metabolism*; D002216:Captopril; D005665:Furosemide; D006801:Humans; D008297:Male; D011188:Potassium / Q000097:blood; D012016:Reference Values; D012083:Renin / Q000097:blood*; D012964:Sodium / Q000097:blood / Q000378:metabolism*
D000809:Angiotensins; D000450:Aldosterone; D005665:Furosemide; D000324:Adrenocorticotropic Hormone; D002216:Captopril; D012964:Sodium; D012083:Renin; D011188:Potassium