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ZHEN-GUO Li, DONALD PARK, FRANK S. LABELLA, Adrenocorticotropin(1–10) and -(11–24) Promote Adrenal Steroidogenesis by Different Mechanisms, Endocrinology, Volume 125, Issue 2, 1 August 1989, Pages 592–596, https://doi.org/10.1210/endo-125-2-592
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Abstract
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 secretogogue. 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.