The sympathetic nervous system and hypertension in primary aldosteronism

To assess the role of the sympathetic nervous system in mineralocorticoid hypertension in humans, results from 24 patients with aldosterone-producing adenoma were compared with those in 27 appropriately matched essential hypertensive subjects and 26 normotensive subjects. Resting plasma catecholamine levels averaged 292 +/- 140 (SD) pg/ml in patients with aldosterone-producing adenoma, 305 +/- 101 in patients with essential hypertension, and 260 +/- 120 in normotensive subjects; none of the differences among the three groups was significant. With head-up tilt (60 degrees for 10 min) plasma catecholamine levels increased similarly in the aldosterone-producing adenoma and essential hypertensive groups (up to 681 +/- 111 and 611 +/- 57 pg/ml respectively, NS). beta-Blockade (propranolol, 10 mg i.v.) in eight aldosterone-producing adenoma patients decreased heart rate (from 78 +/- 5 to 68 +/- 3 beats/min, p less than 0.005) and cardiac output (from 5.5 +/- 0.4 to 4.6 +/- 0.3 liter/min, p less than 0.001), but left mean blood pressure unchanged (127 +/- 4 to 127 +/- 2 mm Hg). Combined alpha- and beta-blockade with phentolamine and propranolol in five patients with aldosterone-producing adenoma produced no detectable changes in blood pressure. Thus, results from biochemical, functional, and pharmacological studies in humans showed no evidence of enhanced peripheral sympathetic activity in the hypertension of primary aldosteronism.