Abstract: | The role of prostaglandins (PGs) in the mechanism of action of acetylcholine (ACh) on frog adrenocortical cells has been examined. Administration of a single dose of ACh (5 × 10−5 M) to perifused frog interrenal fragments, for 20 min, stimulated the production of corticosterone, aldosterone, PGE2 and 6-keto-PGF1α. In contrast ACh did not significantly alter TXB2 production. The effect of ACh could be mimicked by muscarine (10−5 M). Conversely, nicotine (10−6 to 10−4 M) was totally inactive. The increase in PG biosynthesis preceded the peak of corticosteroid release. Repeated 20-min pulses of ACh (5 × 10−5 M) or muscarine (10−5 M) given at 130-min intervales induced a desensitization phenomenon. In presence of indomethacin (5 × 10−6 M), the effect of ACh on PG and steroid secretion was totally abolished. In calcium-free medium, the effect of ACh on PG and corticosteroid production was completely blocked. These results indicated that, in the frog, ACh stimulates corticosteroid secretion through a PG-dependent mechanism. |