Noradrenaline. See

The pathway for synthesis of the catecholamines dopamine, noradrenaline and adrenaline, illustrated in Fig. 8.5, was first proposed by Hermann Blaschko in 1939 but was not confirmed until 30 years later. The amino acid /-tyrosine is the primary substrate for this pathway and its hydroxylation, by tyrosine hydroxylase (TH), to /-dihydroxyphenylalanine (/-DOPA) is followed by decarboxylation to form dopamine. These two steps take place in the cytoplasm of catecholaminereleasing neurons. Dopamine is then transported into the storage vesicles where the vesicle-bound enzyme, dopamine-p-hydroxylase (DpH), converts it to noradrenaline (see also Fig. 8.4). It is possible that /-phenylalanine can act as an alternative substrate for the pathway, being converted first to m-tyrosine and then to /-DOPA. TH can bring about both these reactions but the extent to which this happens in vivo is uncertain. In all catecholamine-releasing neurons, transmitter synthesis in the terminals greatly exceeds that in the cell bodies or axons and so it can be inferred... 

Noradrenaline and adrenaline are the classic catecholamines and neurotransmitters in the sympathetic nervous system. Noradrenaline stimulates the following subtypes of adrenoceptors P, a, U2. It has positive inotropic and chronotropic activities as a result of /3i-receptor stimulation. In addition, it is a potent vasoconstrictor agent as a result of the stimulation of both subtypes (ai,a2) of a-adrenoceptors. After intravenous infusion, its effects develop within a few minutes, and these actions disappear within 1-2 minutes after stopping the infusion. It may be used in conditions of acute hypotension and shock, especially in patients with very low vascular resistance. It is also frequently used as a vasoconstrictor, added to local anaesthetics. Adrenaline stimulates the following subtypes of adrenoceptors /3i, P2, oil, 0L2. Its pharmacological profile greatly resembles that of noradrenaline (see above), as well as its potential applications in shock and hypotension. Like noradrenaline, its onset and duration of action are very short, as a result of rapid inactivation in vivo. Both noradrenaline and adrenaline may be used for cardiac stimulation. Their vasoconstrictor activity should be kept in mind. A problem associated with the use of /3-adrenoceptor stimulants is the tachyphylaxis of their effects, explained by the /3-adrenoceptor downregulation, which is characteristic for heart failure. 

IS0PR0PYL-4-METHYLPYRlMIDYL-0,0-DIETHYL PHOSPHOROTHIOATE see DCM750 ISOPROPYLMETHYLPYRIAnDYL DIETHYL THIOPHOSPHATE see DCM750 ISOPROPYL MYRISTATE see IQNOOO ISOPROPYL NITRATE see IQPOOO ISOPROPYL NITRILE see IJXOOO ISOPROPYL NITRITE see IQQOOO ISOPROPYL NORADRENALINE see DMA 600... 

Examples of secondary causes are Cushing s syndrome, phaeochromocytoma, hyperaldosteronism, renal disease or use of oral contraceptives and corticosteroids. (Phaeochromocytoma is a benign tumour of the adrenal glands resulting in excessive secretion of adrenaline and noradrenaline. See Chapter 6.)... 

Catediolanilnes. Name for the group of biogenic amines derived from l- dopa that are of major significance as neurotransmitters and neurohormones. See under L-adrenaline, dopamine, L-noradrenaline, see also N-acylcatecholamines. 

Catecholamines alkylamino derivatives of pyro-catechol (o-dihydroxybenzene) a group of substances biosynthesized from L-tyrosine, and including the hormones Adrenalin (see), Noradrenalin (see) and Dopamine (see). 

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