Mechanism of action of noradrenaline on secretion of progesterone and oxytocin by the bovine corpus luteum in vitro.
The present studies were conducted: (1) to determine which beta-adrenoceptor subtypes are involved in progesterone and oxytocin (OT) secretion, (2) to examine whether noradrenaline (NA) acts directly on the cytochrome P-450scc and 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), and (3) to study the effect of prostaglandin F2 alpha (PGF2 alpha) on NA-stimulated steroidogenesis in luteal cells. The effect of NA on progesterone secretion from luteal slices of heifers on days 8-12 of the oestrous cycle was blocked by both atenolol (beta 1-antagonist) and ICI 118.551 hydrochloride (beta 2-antagonist). OT secretion was blocked only after treatment with ICI 118.551 hydrochloride (P < 0.05). Dobutamine (10(-4)-10(-6) M), a selective beta 1 agonist and salbutamol (10(-4)-10(-6) M), a selective beta 2 agonist, both increased progesterone production (P < 0.01) with an efficiency comparable to that produced by NA (P < 0.01). The increase of OT content in luteal slices was observed only after treatment with salbutamol at the dose of 10(-5) M (P < 0.01). Dobutamine had no effect on OT production at any dose. A stimulatory effect of NA on cytochrome P-450scc activity (P < 0.05) was demonstrated using 25-hydroxycholesterol as substrate. 3 beta-HSD activity also increased following NA (P < 0.01) or pregnenolone (P < 0.05) and in tissue treated with pregnenolone together with NA (P < 0.01). PGF decreased progesterone synthesis (P < 0.05) and 3 beta-HSD activity (P < 0.01) in tissue treated with NA. We conclude that NA stimulates progesterone secretion by luteal beta 1- and beta 2-adrenoceptors, while OT secretion is probably mediated only via the beta 2-receptor. NA also increases cytochrome P-450scc and 3 beta-HSD activity. PGF inhibits the luteotropic effect of NA on the luteal tissue.
Miszkiel
G
G
Division of Reproductive Endocrinology and Pathophysiology, Institute of Animal Reproduction and Food Research of Polish Academy of Sciences, 10-718 Olsztyn-Kortowo, Poland.
Kotwica
J
J
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000420:Albuterol / Q000494:pharmacology; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D002417:Cattle / Q000502:physiology*; D003338:Corpus Luteum / Q000187:drug effects* / Q000378:metabolism*; D015237:Dinoprost / Q000494:pharmacology; D004280:Dobutamine / Q000494:pharmacology; D005260:Female; D006913:Hydroxysteroid Dehydrogenases / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology*; D010121:Oxytocin / Q000378:metabolism*; D011374:Progesterone / Q000378:metabolism*; D011412:Propanolamines / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D011412:Propanolamines; D004280:Dobutamine; C026777:ICI 118551; D011374:Progesterone; D010121:Oxytocin; D001262:Atenolol; D015237:Dinoprost; D006913:Hydroxysteroid Dehydrogenases; D000420:Albuterol; D009638:Norepinephrine