The Ability of the α2-Adrenergic Agonist Clonidine to Suppress Central Noradrenergic Hyperactivity Secondary to Hemodynamic or Environmental Stimuli

Abstract

Metabolism of catecholamines was monitored by in vivo voltammetry in the ventrolateral medulla (encompassing the A1 group of noradrenergic cell bodies) of anesthetized rats and in the locus coeruleus of behaving rats. Activation of metabolism of catecholamines was produced by using: (1) controlled hypotension (sodium nitroprusside, mean arterial pressure reduced to approximately 60 mm Hg for 60 min, n = 5) in anesthetized animals; and (2) immobilization (10 min) of conscious rats (n = 5). Clonidine, 200 micrograms/kg (i.p., n = 3), suppressed almost entirely the activation of the metabolism of catecholamines secondary to controlled hypotension in the ventrolateral medulla. Clonidine, 50 (n = 3) to 200 (n = 5) micrograms/kg (i.p.), produced a dose-dependent suppression of the activation of the metabolism of catecholamines induced by immobilization in the locus coeruleus of conscious rats. The results obtained from this study provide a biochemical rationale for the use of alpha 2-agonists in conditions where central or peripheral noradrenergic activity is heightened.