Reverse trans-synaptic regulation of neuronal noradrenaline uptake.

It was established that the blocking agent of β-adrenoceptors, propranolol (5.10^?7–1.10^?6 M), activates ³H]noradrenaline uptake by isolated rat organs (vas deferens, spleen, small intestine, atrium, uterus) by 30–180 per cent. The blocking agent of α-adrenoceptors, phentolamine (5.10^?7–1.10^?6M), activates noradrenaline uptake by 30–55 per cent only in the organs possessing postsynaptic α-adrenoceptors (vas deferens, spleen, small intestine). The activator of β-adrenoceptors, isopropylnoradrenaline (5.10^?7–1.10^?6M), was shown to produce a decrease in ³H]noradrenaline uptake by 15–50 per cent in all the organs investigated. The substances activating a-adrenoceptors—urea (2.10^?3–5.10^?3M) and mesatone (1.10^?6–1.10^?5M)—inhibit ³H)noradrenaline uptake in the organs with postsynaptic α-adrenoceptors by 20–45 per cent. Activation of neuronal ³H]noradrenaline uptake induced by phentolamine (1.10^?6M) is due to the release of a humoral factor from the effector cell and its influence on adrenergic neurone. Mesatone (1.10^?5M) causes the formation and release of a humoral factor inhibiting neuronal ³H]noradrenaline uptake. The formation of humoral factors changing the intensity of amine uptake is related to the activation of protein synthesis in the effector cell. The possible mechanism of the reverse trans-synaptic regulation of neuronal noradrenaline uptake via the adrenoceptors of the effector cell is discussed.