Clonidine induced variations of plasma norepinephrine and blood pressure in essential hypertension.

To assess the contribution of sympathetic outflow to blood pressure in patients with essential hypertension, clonidine induced variations of plasma norepinephrine, mean arterial pressure and the pulse rate three hours after a 300 μg dose of oral clonidine, an antihypertensive agent that decreases central sympathetic outflow, were studied. Baseline and clonidine suppressed plasma norepinephrine levels were not significantly different between the normal controls and patients with essential hypertension. The average plasma norepinephrine level, mean arterial pressure and pulse rate were significantly decreased from the baseline value in both normal control and essential hypertension (p<.005). The depressor response to sympathetic inhibition after clonidine were exaggerated in significant proportion in patients with essential hypertension compared to normal control group. Our study suggests that the pressor sensitivity to norepinephrine plays more important role than sympathetic overactivity in some patients with essential hypertension.