Stimulation of 18-hydroxy-11-deoxycorticosterone secretion by angiotensin II and potassium.

The control of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) secretion is incompletely understood: ACTH seems to be the dominant regulator, the importance of angiotensin II (A-II) is uncertain, and the effect of potassium has not been investigated. The purpose of this study was to evaluate the 18-OH-DOC response to these three stimuli in vitro. Suspensions of isolated rat adrenal glomerulosa or fasciculata cells were stimulated with either alpha-1-24 ACTH (0.04 mU/ml), A-II (25 ng/ml), or potassium (5.9 mEq/liter), and 18-OH-DOC production was measured. In glomerulosa cells, ACTH produced the greatest 18-OH-DOC response but A-II and potassium also produced significant (P less than 0.001) 18-OH-DOC increases (control, 162 +/- 14 (SE) ng/10(6) cells incubated; A-II, 368 +/- 39; potassium, 380 +/- 37; ACTH, 1544 +/- 165). In fasciculata cells, 18-OH-DOC production increased with ACTH but not with A-II or potassium. These results document that A-II and potassium, as well as ACTH, can stimulate 18-OH-DOC production by glomerulosa but not by fascicuata cells. The response to A-II may provide an explanation for the reported increase in 18-OH-DOC production after sodium restriction.