The calcium antagonist nimodipine increases beta-endorphin release from rat hypophysis through an action on adrenal glands. An "in vivo" and "in vitro" study.

Intravenous injection of nimodipine (1, 10 and 100 micrograms/Kg) raised plasma ACTH and beta-endorphin (beta-EP) level and reduced pituitary beta-EP content, in the rat. These effects were sharp and short-lasting. Nimodipine (10(-8), 10(-7), 10(-6) M) did not change basal and hypothalamic extract stimulated beta-EP release from pituitary tissue in vitro. Basal release of corticosterone from adrenal glands, superfused in vitro with the calcium antagonist (10(-7) - 10(-6) M), was not modified. However, ACTH-induced release was strongly reduced. Since glucocorticoids feedback regulates biosynthesis and cleavage of pro-opiocortin, nimodipine, which reduces adrenal gland responsiveness to ACTH, might reflexly increase beta-EP release from hypophysis.