Abstract 5943: Sympathetic Overactivity in Hypertensive Patients With Primary Aldosteronism
Increasing animal experimental data indicate that aldosterone increases blood pressure (BP) not only by promoting urinary sodium retention, but also by acting centrally to increase sympathetic vasoconstrictor activity to the peripheral circulation. Although previous studies in patients with primary hyperaldosteronism (PA) provide conflicting evidence, the diagnosis of PA was not confirmed according to the current guidelines. To determine the influence of circulating aldosterone on sympathetic nerve activity (SNA), we compared SNA in 10 hypertensive patients with biochemically proven PA by the salt loading test to 18 patients with essential hypertension (ET) and 14 age-matched normotensive controls (NT) by using direct microneurographic technique. The average urinary aldosterone excretion after 5 days of oral salt loading was 36±8 mcg/day in PA patients. The average BP in PA, ET, and NT was 142±5/88±3, 149±6/88±3, and 120±3/77±2, respectively. We found that SNA was significantly higher in PA patients than NT group (39±4 vs 28±3 bursts/min, p < 0.01) but similar to essential hypertensive patients (38±3 bursts/min, p > 0.05). In subset of 7 PA patients with evidence of a unilateral aldosterone-producing adenoma confirmed by adrenal vein sampling, we repeated measurement of SNA within 6 weeks after removal of their adenoma. SNA decreased significantly in these patients from 38±5 to 27±4 bursts/min (p = 0.01) and BP decreased from 147±4/93±3 to 118±6/75±2 mmHg (p < 0.01). In conclusion, our data in patients with primary aldosteronism provide strong support for a central sympathoexcitatory action of aldosterone in humans.