Absence of Prostacyclin Involvement in Angiotensininduced Aldosterone Secretion in Rat Adrenal Cells*

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Abstract
The role of prostaglandins (PGs) in aldosterone secretion was studied in isolated rat adrenal glomerulosa cells. [14C]Arachidonic acid was metabolized to [14C]6-keto-PGF1.alpha., [14C]PGF2.alpha., [14C]PGE2 and [14C]PGD2. Pretreatment with indomethacin (5 .times. 10-5 M) or U-51605 [1,11-azoprosta-5,13-dienoic acid] (5 .mu.g/ml) inhibited the synthesis of these metabolites. Angiotensin II (AII) stimulated a concentration-related release of aldosterone and 6-keto-PGF1.alpha., but not PGE2. Significant increases in aldosterone and 6-keto-PGF1.alpha. occurred at AII concentrations of 0.2 and 2 nM. The increases in 6-keto PGF1.alpha. concentrations after AII treatment were small, (278 .+-. 33 pg/106 cells .cntdot. h for control vs. 581 .+-. 90 after 2 nM AII). At higher concentrations , AII further stimulated the synthesis of aldosterone and 6-keto PGF1.alpha. in parallel with time of incubation. Indomethacin (3 .mu.M) decreased basal and AII-stimulated aldosterone release by 40% and 23%, respectively, and inhibited the synthesis of PGs. U-51605 (5 .mu.g/ml) failed to alter aldsterone release. Arachidonic acid increased the synthesis of PGE2 and 6-keto-PGF1.alpha. in a concentration-related manner without altering the synthesis of aldosterone. PGH2 stimulated the release of PGE2,6-keto-PGF1.alpha. and aldosterone. PGI2 and PGE2 stimulated aldosterone secretion, which was concentration related. Threshold stimulation by PGI2 and PGE2 occurred at 0.5 and 5 nM, respectively. Maximal stimulation occurred at 5 nM for PGI2 and at 5000 nM for PgE2, with PGE2 producing the greater maximal response. Treatment of the cells with trypsin eliminated the steroidogenic response to PGE2. Apparently, PGI2 and PGE2 are produced by the adrenal glomerulosa cells, and the synthesis of PGI2 may be stimulated by AII. The concentrations of PGI2 synthesized are not adequate to stimulate aldosterone secretion. PGI2 does not appear to mediate angiotensin induced aldosterone secretion.