Stimulation of 32Pi Incorporation into Phosphatidylinositol and Phosphatidylglycerol by Catecholamines and β-Adrenergic Receptor Blocking Agents in Rat Pineal Organ Cultures

摘要: Abstract The effect of norepinephrine, other catecholamines, phenylethylamines, and β-adrenergic receptor blocking drugs on the incorporation 32Pi into phospholipids intact rat pineal glands was studied in organ culture. Individual were assayed for radioactivity after separation by two-dimensional thin layer chromatography. Improved chromatographic separations obtained (Getz, G. S., Jakovcic, Heywood, J., Frank, Rabinowitz, M. (1970) Biochim. Biophys. Acta 218, 441–452), if plates washed with acetone instead ether development first solvent system. Addition l-norepinephrine (0.3 mm) significantly stimulated isotope phosphatidylinositol within 5 min phosphatidylglycerol 15 min. After 3 hours' incubation, phenylethylamine derivatives, including d-norepinephrine, epinephrine, dopamine, tyramine, octopamine (100 to 500%) 200%). Incorporated continued increase up 16 hours, but norepinephrine-induced stimulation steadily declined. stimulating effects essentially linear from 0.3 mm µm. No observed presence N6, O2'-dibutyryl adenosine 3',5'-monophosphate at a concentration as high 10 mm. Several substances widely differing potencies agents, dl,-propranolol, d-propranolol, dichloroisoproterenol, alprenolol, not sotalol, increased acidic phospholipids. However these agents gave labeling pattern different that produced norepinephrine: elevated 1000 1500%, 100%, phosphatidic acid, 50 150%. Neither sotalol nor propranolol prevented phospholipid metabolism caused norepinephrine. These findings indicate is related formation melatonin which cultured either norepinephrine or 3',5'-monophosphate. This conclusion also supported fact fails block enhanced whereas it blocks formation. data further activity brought about through interaction receptors.