Noradrenaline Mimics

Adrenergic drugs are natural or synthetic compounds that either partially or completely replicate the effects of norepinephrine (noradrenaline), epinephrine (adrenaline), and dopamine, and which cause a biological response similar to the activation of the sympathetic nervous system. They are also referred to as sympathomimeties beeause they mimic the stimulation of the sympathetic nervous system. 

SYMPATHOMIMETIC AGENTS mimic the actions of the sympathetic division of the autonomic nervous system. The effects of this system on the tissues and organs are mediated by adrenaline and noradrenaline - which act predominantly as hormone or neurotransmitter, respectively. These catecholamines act at one of two receptor types, a-adrenoceptor and P-adrenoceptor, to exert the actions of the system. Sympathomimetics are of two types. 

Sympathomimetics mimic the action of noradrenaline (norepinephrine), the principal neurotransmitter between the nerve endings of the sympathetic nervous system and the adrenergic receptors of the innervated tissues. They stimulate both alpha-adrenoceptors, causing constriction of smooth muscle and blood vessels, and beta-adrenoceptors, producing bronchodilatation. They are therefore useful in coughs where the tissues of the upper respiratory tract are congested, as they shrink swollen mucosa and open up the airways. 

Sympathomimetic drugs usually mimic stimulation of the peripheral endings of the sympathetic or adrenergic nerves, the action being exerted on the effector cells supplied by postganglionic endings. There is now enough evidence to show that the neurohormone directly concerned with such an action is noradrenaline. 

It is, however, interesting to observe that a good number of sympathomimetics in fact do not really mimic the actions of noradrenaline or adrenaline at the effector receptor. They merely induce the release of noradrenaline from the sympathetic postganglionic adrenergic nerves. Such sympathomimetics which exert their action indirectly are comparatively less effective in patients treated with noradrenaline depleting drugs, for instance, the rauwolfia alkaloids, or other adrenergic neuron blockers. 

Because they mimic the chemical synapse by replacing the receptor cell by a UME, electrochemical techniques involving the artificial synapse configuration are suitable for the real-time monitoring of exocytosis at the single-cell level (see Section 12.1.1) and most particularly because the common neurotransmitters (serotonin [5-hydroxytryptamine] and catecholamines like dopamine, noradrenaline, and adrenaline) can be easily oxidized at carbon surface (E=650 mV versus Ag/AgCl). 

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