Role of prostaglandins in angiotensin-induced steroidogenesis absence of an effect by prostaglandin e₂

Recently, we have found that tbe prostaglandin synthesis inhibitor, indometfaacin, reduced basal and angiotensin stimulated aldosterone release. To further test tbe possibility that prostaglandins (PGs) function as mediators of adrenal steroidogenesis, we examined the release of aldosterone, PGE₂, and PGF_taunder basal and stimulated conditions in isolated adrenal capsular cells in vitro. Angiotensin II and HI caused a dose-related increase in aldosterone release without significantly altering tbe release of PGE, or PGF₂. Indomethacin inhibited basal, angiotensin II, and angiotensin Ill-induced steroidogenesis by 40%, 15%, and 52% respectively. Additionally, it inhibited tbe release of PGE, by 60% in the control and angiotendn-treated cells. In indomethacin-treated cells, PGE, stimulated aldosterone release in sapraphysiologic doses; however, its steroidogenlc effect was not additive with angiotensin II. The prostaglandin precursor, arachidonic acid, increased the adrenal synthesis of PGE, and PGFta in a dose-related manner without altering the synthesis of aldosterone. Similarly, the prostaglandin endoperoxide PGH, increased tbe synthesis of PGE, by 250-fold, yet failed to alter aldosterone synthesis. These findings indicate that PGE, does not mediate or modulate basal or angiotensin-stimulated steroidogenesis. Furthermore, it would appear that indomethacin may inhibit adrenal steroidogenesis via a mechanism other than inhibition of prostaglandin synthesis.