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.
D000311:Adrenal Glands / Q000502:physiology*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D003345:Corticosterone / Q000378:metabolism; D004723:Endorphins / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D009539:Nicotinic Acids / Q000494:pharmacology*; D009553:Nimodipine; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D001615:beta-Endorphin
D002121:Calcium Channel Blockers; D004723:Endorphins; D009539:Nicotinic Acids; D009553:Nimodipine; D001615:beta-Endorphin; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone