Vinson G P, Teja R, Ho M M, Hinson J P, Puddefoot J R
Department of Biochemistry, St. Bartholomew's, London, UK.
Endocr Res. 1996 Nov;22(4):589-93. doi: 10.1080/07435809609043751.
The tissue renin angiotensin systems (RAS) may have specific roles that complement those of the systemic RAS. In the adrenal, the tissue RAS has been implicated in mediating the response of the tissue to stimulation by ACTH and potassium ions, but its role in the response to angiotensin II stimulation has not been addressed. To examine this, rat adrenals were incubated either as bisected glands or as separated capsular glands (largely glomerulosa) under control conditions, or in the presence of the angiotensin converting enzyme inhibitor captopril, or of angiotensin II, or both. Captopril inhibited the two different tissue preparations in different ways. In the capsular gland it inhibited basal aldosterone output, but facilitated its response to angiotensin II. In the bisected gland, captopril inhibited the response of aldosterone to angiotensin II. The results illustrate the importance of the tissue RAS in the synthesis of aldosterone and the response to angiotensin II, and the two sets of data suggest that the fasciculata and glomerulosa zones interact in the formation of aldosterone. One way in which this may occur is by the mobilisation of fasciculata synthesised substrate, such as 18-hydroxydeoxycorticosterone (18-OH-DOC), for conversion by the glomerulosa, which is apparently supported by endogenous angiotensin II.
