Abstract 2583: Dietary Salt Modulates the Hypertensive Effect of High Aldosterone in Subjects with Resistant Hypertension
Introduction: Aldosterone excess raises blood pressure levels and contributes to injury in target organs including the heart, kidneys, and brain. Experimental data suggest that the deleterious effects of aldosterone are dependent upon concomitant high dietary salt ingestion. However, no human studies have evaluated the interaction between dietary salt and hyperaldosteronism.
Hypothesis: We tested the hypothesis that ambulatory blood pressure levels are related to the interaction of dietary salt and aldosterone in subjects with resistant hypertension.
Methods: One hundred thirty-six subjects with resistant hypertension were prospectively evaluated by measurement of 24-hour urinary aldosterone (Ualdo) and sodium (UNa), and 24-hr ambulatory blood pressure monitoring (ABPM). Daytime, nighttime and 24-hr blood pressure (BP) as well as nocturnal blood pressure decline were determined. Subjects were designated as having high (Ualdo≥12 μg/24h) or normal (Ualdo<12 μg/24h) aldosterone excretion. Subjects were further divided into 3 groups according to urinary salt excretion: low (Una<125 mEq/24h), medium (125≤Una<225 mEq/24h), and high (Una≥225 mEq/24h).
Results: Overall, the mean office blood pressure was 160.2/89.8 mmHg on an average of 4.1 medications. There was no difference in mean office BP values between the 72 subjects with normal Ualdo and the 64 subjects with high Ualdo. There was no difference in office and 24-hr BP levels in the normal Ualdo group regardless of urinary sodium excretion. In contrast, in the high Ualdo group, the office diastolic (89.2±2.7 vs 78.5±2.9mmHg, p=0.03), systolic daytime (149.0±3.2 vs 136.8±4.1mmHg, p=0.03), diastolic daytime (86.9±2.2 vs 77.3±2.9 mmHg, p=0.01), systolic nighttime (143.1±3.2 vs 127.7±5.4 mmHg, p=0.01), diastolic nighttime (81.4±2.3 vs 69.4±3.6 mmHg, p=0.006), 24-hour systolic (146.8±3.0 vs 133.4±4.1mmHg, p=0.01), and 24-hour diastolic (84.6±2.1 vs 74.5±3.2mmHg, p=0.01) BP were all higher in high compared to low urinary sodium excretion group.
Conclusion: Reduced dietary salt ingestion blunts the hypertensive effects of high aldosterone levels. This is the first demonstration that dietary salt ingestion significantly modulates the clinical effects of aldosterone in humans.