Abstract
There are a variety of regulatory factors in the control of the biosynthesis of the neurotransmitter noradrenaline and the adrenal medullary hormone adrenaline. Increased sympathoadrenal activity causes an immediate increase in the formation of noradrenaline from tyrosine in the sympathetic nerve terminals [Alousi and Weiner, 1966 ; Sedvall and Kopin, 1967 (1)] and in the adrenal medulla (Gordon et al., 1966). This rapid change in catecholamine synthesis is due to an end-product inhibition of tyrosine hydroxylase (Spector et al., 1967) and/or an increase of cofactor or substrate concentration [Sedvall and Kopin, 1967 (2)]. In spite of the more rapid conversion of tyrosine to noradrenaline after increased activity of the sympathetic nervous system, no elevation in the in vitro activity of tyrosine hydroxylase activity has been observed (Thoa and Kopin, personal communication). Recent work in our laboratory has shown that the synthesis of tyrosine hydroxylase, the rate limiting step in the catecholamine biosynthesis (Levitt et al., 1965) and phenylethanolamine N-methyltransferase (PNMT), the final step in adrenaline formation, is regulated by the activity of the sympathetic nervous system and by pituitary and corticoid hormones.
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Axelrod, J., Mueller, R.A., Thoenen, H. (1970). Neuronal and Hormonal Control of Tyrosine Hydroxylase and Phenylethanolamine N-Methyltransferase Activity. In: Schümann, HJ., Kroneberg, G. (eds) New Aspects of Storage and Release Mechanisms of Catecholamines. Bayer-Symposium, vol 2. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-46241-2_19
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DOI: https://doi.org/10.1007/978-3-642-46241-2_19
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