Effects of clonidine on sympathetic function.
Fifteen patients with essential hypertension and ten with pheochromocytoma were studied to assess the effect of clonidine, a centrally acting antihypertensive agent, on the functional and biochemical indices of sympathetic function. Single oral doses of clonidine (0.3 mg) decreased supine plasma norepinephrine significantly in essential hypertension, but not in pheochromocytoma despite producing similar reductions in blood pressure and heart rate. Plasma renin activity was unchanged in both groups. In untreated essential hypertension, head-up tilt increased diastolic blood pressure, heart rate, and plasma norepinephrine. Three hours after a single oral dose of clonidine, head-up tilt resulted in significant blood pressure reductions, although heart rate and plasma norepinephrine increased dramatically. Clonidine might reduce blood pressure by inhibiting sympathetic outflow, and any effect on plasma renin activity appears unimportant in its antihypertensive action. In pheochromocytoma clonidine decreases blood pressure without altering plasma norepinephrine, which is consistent with the concept that the norepinephrine released from axon terminals of sympathetic postganglionic neurons is biologically more significant than circulating catecholamines.
D000310:Adrenal Gland Neoplasms / Q000188:drug therapy*; D001794:Blood Pressure / Q000187:drug effects; D003000:Clonidine / Q000627:therapeutic use*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D010673:Pheochromocytoma / Q000188:drug therapy*; D011187:Posture; D012083:Renin / Q000097:blood; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000503:physiopathology
D012083:Renin; D003000:Clonidine; D009638:Norepinephrine