Catecholamine stimulation ephedrine

Kaye and Fainstat 1987 Wooten et al. 1983). The risk of cerebral hemorrhage is even greater when combining ephedrine with other catecholamine stimulants such as the over-the-counter stimulant phenyl-propanolamine (StoessI et al. 1985). Pseudoephedrine may be safer than ephedrine in some respects (Porta et al. 1986). In a large sample (n > 100,000) of pseudoephedrine users, there were no reports of cerebrovascular disorders within 15 days after administration. The incidence of myocardial infarction, seizures, and neuropsychiatric disorders were no greater than base rates in the general population. 

Considering the chemical structure of ephedrine, it is interesting to observe the lack of the phenolic group, characteristic of catecholamines. However, ephedrine remains capable to stimulate a- and p-receptor directly and displace norepinephrine (NE) from storage vesicles, releasing these catecholamines at synaptic areas in the brain and in the heart. These released substances act on receptors promoting the adrenergic effect [17, 66]. 

Ephedrine and pseudoephedrine share properties with cocaine and with the amphetamines because they (1) stimulate (3-receptors directly, and (2) also cause the increased release of norepinephrine. Chronic exposure to abnormally high levels of circulating catecholamines can damage the heart. This is certainly the case with cocaine and methamphetamine (116,117), but ephedrine-related cardiomyopathy is an extremely rare occurrence, occurring only in individuals who take massive amounts of drug for prolonged periods of time. Only two papers have ever been published on the subject (118,119). 

Indirecdy acting sympathomimetics release noradrenaline from the nerve endings and/or inhibit its re-uptake. Thereby, the noradrenaline concentration in the synaptic cleft is raised, and the sympathetic tone therefore increased. After repeated administration of higher doses, this effect is however restricted by the limited supply of newly synthesised noradrenaline. Typical representatives are ephedrine and the amphetamines (Fig. 6.39). The high polarity of catecholamines, associated with the two aromatic hydroxyl-groups, necessitates intravenous administration, and confines their activity to the periphery. Ephedrine, amphetamine, and as well methamphetamine exhibit in addition to their peripheral sympathomimetic effect also a central stimulating activity. 

The stimulation of adrenergic preceptors is accomplished by three types of sympathomimetics the epinephrine-type which directly stimulates preceptors in the airways as well as o-receptors in the blood vessels the ephedrine-type. which indirectly stimulate p and o-receptors by releasing catecholamines and the isoproterenol-type, which directly stimulate preceptors but not preceptors. 

The hormones are stored in special granules which are present in the sympathetic nerve endings and medullary cells and the net hormonal output depends on the rates of both the synthesis and release. Any catecholamine that diffuses from the synapse into the remainder of the neuron is destroyed by a monoamine oxidase. Sympathomimetic drugs such as ephedrine and the amphetamines act by inhibiting monoamine oxidase and slowing the removal of catecholamines and 5-hydroxytryptamine (serotonin) from within neurons. In this way they increase the sensitivity of the neuron to stimulation and act as antidepressants. Any catecholamines that are released into the bloodstream are rapidly removed and inactivated by the liver. 

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