Dietary Salt Intake and the Clonidine Suppression Test

We studied the effects of one week of dietary salt restriction and one week of salt loading on hemodynamic and plasma catecholamine responses to clonidine. Among 11 outpatients with essential hypertension, urinary sodium excretion averaged 29 mEq/d during salt restriction and 322 mEq/d during salt loading. Among eight inpatient normotensive subjects, urinary sodium excretion averaged 11 mEq/d during salt restriction and 300 mEq/d during salt loading. Three hours after administration of oral clonidine 300 μg, the hypertensive patients had an average (± one standard deviation) decrease in mean arterial pressure of 20 ± 6% while receiving the low salt diet and 19 ± 9% while taking the high salt diet, with decreases in venous plasma norepinephrine (NE) of 61 ± 15% and 61 ± 16%, respectively. The normotensive subjects had a decrease in mean arterial pressure of 16 ± 8% with the low salt diet and 15 ± 9% with the high salt diet, with decreases in venous plasma NE of 64 ± 10% and 66 ± 8%. Thus, in neither group were the percent decreases in plasma NE or in mean arterial pressure after clonidine affected by diet. Short‐term, large‐magnitude changes in dietary intake of sodium do not affect the sympathetic contribution to blood pressure as indicated by percent responses of plasma NE or of mean arterial pressure to clonidine administration. 1987 American College of Clinical Pharmacology