We identified eight hypertensive patients who developed severe bradycardia during oral clonidine hydrochloride therapy. Seven patients had sinus bradycardia, four had long sinus pauses, two had junctional bradycardia, and two had high-degree atrioventricular block. Three populations at risk for severe bradycardia during oral clonidine therapy were identified: patients with renal insufficiency, patients with clinical sinus node dysfunction, and patients who had developed bradycardia while taking other sympatholytic agents or who were currently receiving another sympatholytic drug. Clonidine effects were dissociated in two patients who were not hypotensive despite severe bradycardia. Asymptomatic patients required only dose reduction or discontinuation of clonidine therapy. Symptomatic patients responded inconsistently to intravenous atropine sulfate therapy; one responded to isoproterenol therapy, and one required temporary artificial pacing. Awareness of the variable presentation and response of this bradycardia to medical therapy will assist patient management. The incidence of this complication is low (less than 0.3%), but attention to risk factors should make clonidine-induced bradycardia even less frequent.