[Analysis of the regulatory influence of effector cells on 3H-catecholamine synthesis in an adrenergic neuron].
In isolated organs of the white rats activation of noradrenaline-H3 and dophamine-H3 synthesis during action of the alpha-adrenoblocking agent phentolamine (1.10(-6) M) and inhibition of the amines synthesis under influence of the alpha-adrenoreceptor activator mezaton (1.10(-5) M) were due to a release from cells-effectors of respective humoral factors and to the latters' effect upon the processes of amine formation in the adrenergic neuron. Formation of the humoral factors altering the rate of catecholamines-H3 synthesis is associated with activation of the protein synthesis in cells-effectors and occurs during change of the functional state (excitation or blockade) of the post-synaptic adrenoreceptors. The processes occurring at the time in the adrenergic neuron, are not correlated with protein formation. The possibility of existence of a common mechanism for feed-back transsynaptic regulation of synthesis and neuronal uptake of noradrenaline via adrenoreceptors of cells-effectors by means of changing the intensity of thyrosin and noradrenaline transport into the neuron is discussed.
D000320:Adrenergic Fibers / Q000378:metabolism*; D000818:Animals; D003513:Cycloheximide / Q000494:pharmacology; D004298:Dopamine / Q000096:biosynthesis*; D006321:Heart / Q000294:innervation; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009638:Norepinephrine / Q000096:biosynthesis*; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011941:Receptors, Adrenergic / Q000502:physiology*; D014649:Vas Deferens / Q000294:innervation
D011941:Receptors, Adrenergic; D010656:Phenylephrine; D003513:Cycloheximide; D011433:Propranolol; D007545:Isoproterenol; D004298:Dopamine; D009638:Norepinephrine; D010646:Phentolamine
Analiz reguliatornogo vliianiia éffektornoĭ kletki na sintez katekholaminov-H3 v adrenergicheskom neĭrone.