Peripheral sympathetic systems, inhibitors

Cholinesterase inhibitors have minimal effects by direct action on vascular smooth muscle because most vascular beds lack cholinergic innervation (coronary vasculature is an exception). At moderate doses, cholinesterase inhibitors cause an increase in systemic vascular resistance and blood pressure that is initiated at sympathetic ganglia in the case of quaternary nitrogen compounds and also at central sympathetic centers in the case of lipid-soluble agents. Atropine, acting in the central and peripheral nervous systems, can prevent the increase of blood pressure and the increased plasma norepinephrine. 

MAO Inhibitors. In contrast to the tricyclics, MAO inhibitors tend to produce CNS excitation, which can result in restlessness, irritability, agitation, and sleep loss. These drugs also produce some central and peripheral anticholinergic effects (e.g., tremor, confusion, dry mouth, urinary retention), but these effects tend to occur in a lesser extent than with the tricyclics (see Table 7-3). Because of the systemic MAO inhibition, excess activity at peripheral sympathetic adrenergic terminals may cause a profound increase in blood pressure, leading to a hypertensive crisis. This situation is exacerbated if other drugs that increase sympathetic nervous activity are being taken... 

Amine uptake blockade The drugs that block norepinephrine transporters in the CNS (eg, tricyclics) also inhibit the reuptake of norepinephrine at nerve endings in the autonomic nervous system. Likewise, MAO inhibitors increase NE in sympathetic nerve terminals. In both cases, this can lead to peripheral autonomic sympathomimetic effects. However, longterm use of MAOIs can decrease blood pressure. 

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