Noradrenaline synthesis and utilization: Control by nerve impulse flow under normal conditions and after treatment with alpha-adrenoreceptor blocking agents

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Abstract
The changes in the synthesis and utilization of noradrenaline cranial and caudal to an acute section of the rat spinal cord have been used to investigate the importance of nerve impulses for these processes. 1. Cranial to a lesion of the spinal cord, the α-methyltyrosine-induced disappearance of noradrenaline was accelerated by the α-adrenoreceptor blocking agents yohimbine (10 mg/kg), piperoxan (60 mg/kg) and tolazoline (50 mg/kg). In the absence of nerve impulses caudal to a lesion of the spinal cord, this disappearance was decelerated as compared to that cranial to the lesion and it was not influenced by the three α-adrenoreceptor blocking agents. 2. The nialamide-induced accumulation of normetanephrine in the whole brain was increased by phenoxybenzamine (20 mg/kg) and yohimbine whereas it was decreased by the α-adrenoreceptor stimulating agent clonidine (0.1 mg/kg). The effect of clonidine was completely antagonized by yohimbine, but not by phenoxybenzamine, giving further evidence for the view that clonidine and yohimbine have a stronger effect than phenoxybenzamine on the α-adrenoreceptors regulating the release of noradrenaline induced by nerve impulses. 3. The accumulation of Dopa after decarboxylase inhibition cranial to a lesion of the spinal cord was accelerated by yohimbine, piperoxan and tolazoline, but not significantly affected by phenoxybenzamine and haloperidol (10 mg/kg). In the absence of nerve impulses caudal to a lesion of the spinal cord, the Dopa accumulation was decelerated as compared to that cranial to the lesion and it was not influenced by the former three α-adrenoreceptor blocking agents as well as by clonidine. 4. The results show that the synthesis and the utilization of noradrenaline normally, as well as the accelerations of these processes by α-adrenoreceptor blocking agents, are dependent on nerve impulses. The stimulation of the synthesis and utilization of noradrenaline by nerve impulses might be influenced via the activity of the α-adrenoreceptors located either on the nerve terminals or on the cell bodies or on both parts of the noradrenergic neurones. In the absence of nerve impulses, a receptor-mediated feed-back mechanism similar to that described for the synthesis of dopamine does not appear to regulate the synthesis of noradrenaline.

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