Reverse trans-synaptic regulation of catecholamine synthesis in adrenergic neurones.

It was established that the blocking agent of beta-adrenoceptors, propanolol (1 X 10(-6)M), activates [3H] catecholamine synthesis from [3H] tyrosine in isolated rat organs (vas deferens and atrium) by 40-80%. The blocking agent of alpha-adrenoceptors, phentolamine (1 X 10(-6)M) activates [3H] catecholamine synthesis by 30-60% only in the organ possessing postsynaptic alpha-adrenoceptors (vas deferens). The activator of beta-adrenoceptors, isopropylnoradrenaline (1 X 10(-6)M), was shown to produce a decrease in [3H] catecholamine synthesis by 30-40% in both organs investigated. The substance activating alpha-adrenoceptors, phenylephrine (1 X 10(-5)M), inhibits [3H] catecholamine synthesis in the organ with postsynaptic alpha-adrenoceptors by 40-50%. Activation and inhibition of [3H] catecholamine synthesis induced by adrenotropic drugs is due to the release of chemical factors from he effector cell and their influence on the adrenergic neurone. The formation of chemical factors changing the intensity of catecholamine synthesis is related to the activation of protein synthesis in the effector cell. The processes which proceed in the adrenergic neurone are not connected with protein synthesis de novo. Existence of the common mechanism for trans-synaptic regulation of noradrenergic synthesis and uptake via the adrenoceptors of the effector cell is discussed.