Adrenocorticotropin(1-10) and -(11-24) promote adrenal steroidogenesis by different mechanisms.

ACTH1-10 and ACTH11-24 each elicit cortisol secretion submaximally in freshly dispersed or cultured beef adrenal cortical cells. The combination of ACTH1-10 and ACTH11-24 promotes cortisol release to the maximal level elicited by ACTH1-24. Maximal cortisol release by ACTH11-24, but not by ACTH1-24 or ACTH1-10, was enhanced by forskolin. The calcium channel blockers nifedipine and verapamil inhibited cortisol release by ACTH1-10, ACTH1-24 or ACTH11-24, suggesting calcium influx to be essential for steroid secretion regardless of the secretagogue. Vanadium, in a dose-dependent manner, inhibited cortisol secretion elicited by ACTH1-24 and ACTH1-10 but not that caused by ACTH11-24. These results suggest that there are at least two receptors mediating ACTH1-24-dependent steroid secretion. One class of receptor recognizes ACTH1-10 but not ACTH11-24 and is linked to the cAMP messenger pathway.