Elevated sympathetic nerve activity in borderline hypertensive humans. Evidence from direct intraneural recordings

Abstract

Reports of elevated plasma catecholamine levels and augmented responses to autonomic blockade suggest increased sympathetic tone in borderline hypertension. It is not known if this reflects greater sympathetic neural outflow. We directly recorded muscle sympathetic nerve activity (microneurography) in 15 normotensive and 12 borderline hypertensive age-matched men to determine whether borderline hypertensive individuals have elevated sympathetic nerve activity. Supine heart rate, blood pressure, plasma norepinephrine, and efferent muscle sympathetic nerve activity (peroneal nerve) were measured after 6 days of both low and high dietary sodium intake (10 and 400 meq sodium/24 hr). Sympathetic nerve activity was elevated significantly in borderline hypertensive individuals on both low (37 ± 1 in borderline hypertensive individuals vs. 29 ± 1 bursts/min in normotensive individuals; p < 0.01) and high (25 + 1 in borderline hypertensive individuals vs. 16 ± 1 bursts/min in normotensive individuals; p < 0.01) sodium diets. The borderline hypertensive group had higher systolic (p < 0.01) and diastolic (p < 0.05) blood pressures independent of sodium intake. Across both groups, high sodium intake reduced muscle sympathetic nerve activity (p < 0.001), plasma norepinephrine (p < 0.001), diastolic blood pressure (p < 0.02), heart rate (P < 0.002), and increased weight (p < 0.005). A significant (p < 0.05) group-by-diet interaction was observed for plasma norepinephrine levels. Specifically, compared with the normotensive group, plasma norepinephrine levels in the borderline hypertensive group tended to be higher on low sodium diet (p = 0.08) and lower on high sodium diet (p = 0.23). High sodium intake increased diastolic pressure by over 5 mm Hg in six of 27 subjects (four borderline hypertensive and two normotensive). Sympathetic activity in sodium-sensitive subjects was not elevated compared with sodium-resistant subjects and also declined during high sodium intake. This study supports the hypothesis of elevated central sympathetic neural outflow in borderline hypertension.