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Result Grossman et al., 1991 ; . Conversely, the combination of a high plasma norepinephrine level and a large fall in blood pressure in response to clonidine may identify patients with "hypernoradrenergic hypertension" Goldstein et al., 1985 ; . Yohimbine exerts effects opposite to those of clonidine. Intravenous infusion of yohimbine increases sympathetic neural outflows and blocks 2-adrenoceptors on sympathetic nerve terminals, thereby increasing plasma norepinephrine levels. Yohimbine challenge testing can assess whether a patient with neurogenic orthostatic hypotension has releasable norepinephrine stores Robertson et al., 1986 ; , which can be a target for treatment. Yohimbine challenge testing can also reveal excessive norepinephrine release in patients with anxiety or panic disorder Charney et al., 1984 ; . Indirectly acting sympathomimetic amines, such as dextroamphetamine and tyramine, release norepinephrine from sympathetic nerve endings. These drugs are substrates for both the cell membrane norepinephrine and vesicular monoamine transporters. By intravesicular alkalinization, they enhance norepinephrine leakage from storage vesicles into the axoplasm. They also interfere with the efficiency of the cell membrane norepinephrine transporter, resulting in transport of the axoplasmic norepinephrine into the extracellular fluid. In humans, infusion of tyramine or dextroamphetamine therefore increases plasma norepinephrine levels. During tyramine infusion, plasma DHPG levels increase to a proportionately larger extent than do plasma norepinephrine levels Goldstein and Holmes, 1997 ; , probably because of the greater buildup of norepinephrine in the axoplasm than in the extracellular fluid. Foodstuffs such as hard cheeses and red wines contain large amounts of tyramine. Normally, dietary tyramine is metabolized in the gastrointestinal tract and liver before the amine can enter the systemic circulation. In patients taking an MAO inhibitor, tyramine is able to reach the sympathetic nerve terminals, and after neuronal and vesicular uptake of tyramine, paroxysmal hypertension can result from release of vesicular norepinephrine--a phenomenon termed the "cheese effect". Because of the susceptibility to severe hypertension due to the cheese effect, MAO inhibitors have not had wide usage as antidepressants, despite their clinical efficacy. -Methyl-para-tyrosine Demser; Merck, Whitehouse Station, NJ ; blocks tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis. Repeated administration of -methyl-para-tyrosine decreases plasma levels of DOPA, DOPAC, norepinephrine, and DHPG. The drug is used clinically before surgery to remove a pheochromocytoma. Carbidopa inhibits L-aromatic-amino acid decarboxylase, which catalyzes conversion of levodopa to dopamine. Since carbidopa does not pass through the blood-brain barrier, administration of carbidopa with levodopa increases delivery of levodopa to the brain, while decreasing nausea and vomiting resulting from production of dopamine from levodopa outside the brain hence the brand name "Sinemet" from the Latin for "without vomiting" for the combination of levodopa carbidopa ; . Carbidopa increases plasma levels of endogenous DOPA and decreases renal dopamine production from circulating DOPA.

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