The response of the adrenals from rat fetuses at 16,18 and 20 days of gestation to 1–24 ACTH and α-melanocyte-stimulating hormone (α-MSH) was studied in vitro. The response to 1–24 ACTH increased as gestation progressed. By the end of fetal life, corticosterone release induced by ACTH from whole adrenals was greater than that observed with adrenal tissue from non-pregnant adult female rats. High doses of α-MSH also stimulated adrenal activity but the response to ACTH was always higher than that to α-MSH.
The effect of 1–24 ACTH and α-MSH on fetal adrenal growth was also compared in vivo. The adrenal atrophy induced by fetal hypophysectomy on day 17 of gestation could be prevented by i.m. administration of 10 μg 1–24 ACTH or α-MSH. However, the adrenal growth was greater in ACTH-treated fetuses than in α-MSH-treated ones. Later in gestation, between days 19 and 20, 1–24 ACTH but not α-MSH was able to prevent atrophy induced by fetal hypophysectomy.
These findings are discussed in relation to the literature on levels of ACTH and α-MSH in the plasma and pituitary glands of the rat throughout the last third of gestation. High levels of ACTH in the fetal circulation contrast sharply with very weak or undetectable concentrations of α-MSH. Since the present data suggest that both trophic and steroidogenic activities of ACTH were greater than those of α-MSH, it may be concluded that ACTH but not α-MSH plays a major physiological role during gestation in the regulation of both fetal adrenal growth and function in the rat.
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