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The intracellular mechanisms of action of -MSH in rat adrenocortical cells were examined. When rat adrenal capsule (largely glomerulosa) cells were stimulated with a range of concentrations of -MSH there was significant stimulation of aldosterone secretion at 10^-10 mol/l, although cyclic AMP was not increased until high concentrations of -MSH were used (10^-6 mol/l and above). However, cells incubated with ACTH showed an increase in aldosterone secretion at 10^-11 mol/l and levels of cyclic AMP were elevated at 10^-9 mol ACTH/1.

When rat adrenal whole capsules were incubated with -MSH, membrane-bound protein kinase C (PKC) activity was increased and cytosolic enzyme activity decreased, showing PKC activation. Stimulation with angiotensin II also induced translocation of PKC activity, but ACTH did not.

When [³H]inositol-loaded glomerulosa cells were stimulated with -MSH there was significant generation of [³H]inositol trisphosphate (IP₃) at concentrations of -MSH which stimulated secretion of aldosterone. Significantly increased levels of [³H]IP₃ were also measured when loaded cells were exposed to angiotensin II. ACTH did not cause any significant stimulation of [³H]IP₃ production at any concentration used. These results indicate that activation of PKC and phospholipase C is important in modulating the steroidogenic effect of -MSH.