Sympathomimetic drug

The above categories of autonomic drugs have been treated separately, including typical examples from each group. 

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. 

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. 

A few important compounds used as sympathomimetic drugs are discussed below ephedrine epinephrine adrenaline isoprenaline methoxamine hydrochloride metarminol bitartrate naphazoline hydrochloride oxymetazoline hydrochloride phenylpropanolamine hydrochloride xylometazoline hydrochloride, etc. 

Nagai first isolated ephedrine in 1887 from a well-known Chinese herb, ma huang by moistening the powdered drug with either aqueous sodium carbonate or with lime water and subsequently extracting it with ethanol or benzene. 

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Additive sympathomimetic effects may develop when decongestants are administered with other sympathomimetic drug s (see Chap. 22). Use of the nasal decongestants with the MAOIs may cause hypertensive crisis. Use of a decongestant with beta-adrenergic blocking dragp may cause hypertension or bradycardia. When ephedrine is administered with theophylline, the patient is at increased risk for theophylline toxicity. 

Sympathomimetics (drugs that mimic the sympathetic nervous system) are used primarily to treat reversible airway obstruction caused by bronchospasm associated with acute and chronic bronchial asthma, exercise-induced bronchospasm, bronchitis, emphysema, bronchiectasis (abnormal condition of the bronchial tree), or other obstructive pulmonary diseases. 

Q Anxiety related to adverse reactions ot the bronchodilators (sympathomimetic drugs)... 

MAO Is have not been evaluated systematically for treatment of PD under the current diagnostic classification and generally are reserved for patients who are refractory to other treatments.48,49 MAOIs have significant side effects that limit adherence. Additionally, patients must adhere to dietary restriction of tyramine and avoid sympathomimetic drugs to avoid hypertensive crisis. 

Derivatives of phenylethanolamine substituted by a phenolic hydroxyl on the para position have been known for some time to exhibit 0-adrenergic agonist activity. As a consequence of this property, the compounds have proven useful as bronchodilators for the treatment of asthma (see Chapter 3). Since such sympathomimetic drugs tend to have undesired activity on the cardiovascular system in addition to the desired activity on the bronchii, considerable work has been devoted to the preparation of compounds that would show selectivity for the adrenergic receptors (02> that predominate in the lung. Attachment of the side chain to a heterocyclic aromatic phenol has been one avenue that has shown promise for achieving this selectivity. 

Hoffman, B.B., Adrenoceptor-activating and other sympathomimetic drugs, in Basic and Clinical Pharmacology, 8th ed., Katzung, B.G., Ed., Lange Medical Books/McGraw-Hill, New York, 2001, chap. 9. 

In addition to this serious diet-drug interaction, irreversible MAOIs also potentiate the effects of sympathomimetic drugs like ephedrine found in over-the-counter cold remedies and recreational stimulants like amphetamine. The MAOIs also interact with drugs that increase synaptic concentrations of 5-HT, such as the tricyclic antidepressant clomipramine and the herbal SSRI antidepressant St John s wort (Hypericum spp.). The resulting serotonin syndrome is characterised by hyperthermia and muscle rigidity. While devoid of these side effects the reversible MAO-A inhibitor moclobemide has yet to establish itself as a first-line alternative to the SSRIs. 

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. 

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