Regulation of adenylate cyclase activity in hamster adipocytes. Inhibition by prostaglandins, alpha-adrenergic agonists and nicotinic acid.

摘要: In ghosts of hamster adipocytes, the regulation adenylate cyclase (ATP: pyrophosphate lyase, cyclizing; EC 4.6.1.1) activity by prostaglandins, α-adrenergic agonists and nicotinic acid was studied. These three classes antilipolytic agents caused inhibition without an apparent lag phase. Maximal inhibitions observed ranged between about 45% (by agonists) 60% prostaglandins acid). The order potency for inhibitory (PG) PGE1 ≧ PGE2>PGF2α≅PGI2>PGD2>6-keto PGF1α. IC50 values obtained were 0.007, 0.06, 0.3 1 μM PGE1, PGF2α, PGD2 6-keto PGF1α, respectively. α-Adrenergic agonists, studied in presence β-adrenergic blocking agent, propranolol (30 μM), inhibited fat cell enzyme with (1)-adrenaline > (1)-α-methylnoradrenaline ≅ (1)-noradrenaline clonidine tetryzoline (1)-phenylephrine. 3 10 μM, effect blocked antagonists yohimbine phentolamine prazosin. findings suggest that α2 receptors is involved this catecholamine-induced inhibition. Nicotinic (10 μM) reduced half-maximal effectiveness at 0.6 μM. derivatives, nicotinamide, β-pyridylcarbinol NAD (up to 100 had no on activity.