Administration of the anti-hypertensive agent clonidine as a single (0.5 mg) oral dose or as multiple doses (0.2-0.4 mg/day for 4 days) markedly reduced plasma catecholamines (decrement = 81 ± 3% and 68 ± 5%, respectively, X ± SE, % of basal; both P<0.001) in normal male volunteers. Five patients with various metabolic disorders showed similar responses. The absolute decrements in plasma catecholamines correlated significantly with basal catecholamine levels (P<0.001). Clonidine-induced decrements in mean arterial blood pressure correlated significantly with decrements in plasma catecholamines (P<0.001). The clonidine effect upon catecholamine levels was reversed by phentolamine (clonidine = -68 ± 5%; clonidine with phentolamine = -1 ± 16%). The decrements in catecholamines induced by clonidine in normal subjects were associated with increased sensitivity to the pressor effect of infusion of exogenous norepinephrine. In an analogous fashion flushing associated with endogenous adrenergic discharge was blocked by clonidine, whereas that due to exogenous catecholamines was intensified. These data are compatible with data in experimental animals suggesting that clonidine acts at least in part by interaction with a central alpha adrenergic receptor.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Clinical Endocrinology and Metabolism|
|State||Published - 1978|