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Text sizeChicago, IL - Results of a new study suggest that reduced sodium intake can protect against endothelial dysfunction caused by high aldosterone in patients with resistant hypertension.
The study was presented at the American Heart Association 58th Annual High Blood Pressure Research Conference.
Although the link has been shown in animal studies, this study is the first demonstration in humans that reduced sodium intake can protect against aldosterone-induced vascular dysfunction, said lead author Dr David A Calhoun (University of Alabama at Birmingham).
"More and more, we and others are suggesting and have documented that high aldosterone does contribute to development of hypertension, particularly resistant hypertension," Calhoun told heartwire. This study suggests reducing salt intake may mitigate the ill effects of high aldosterone.
Hold the salt
Calhoun and colleagues had previously reported that a chronic excess of aldosterone, a hormone that affects BP and salt balance, induces endothelial dysfunction measured by brachial-artery flow-mediated dilation (FMD) in patients with resistant hypertension, defined as hypertension uncontrolled by three or more medications.
This study aimed to assess whether low sodium ingestion in the setting of high aldosterone can protect against aldosterone-induced endothelial dysfunction. In 120 patients with resistant hypertension seen consecutively at their institution, the researchers first evaluated plasma renin activity and 24-hour urinary aldosterone and sodium excretion during routine salt intake. Brachial-artery FMD was measured in all subjects.
Of these, 34 were found to have aldosteronism, defined as suppressed plasma renin activity (<1.0 ng/mL per hr) and elevated aldosterone excretion (>12 g/24 hr). In these subjects, they found a strong negative correlation between FMD and urinary sodium excretion, as well as the product of urinary aldosterone and sodium, suggesting better endothelial function among those with lower sodium intakes.
When patients were divided on the basis of urinary sodium excretion above and below 150 mEq/24 hr, those with low sodium excretion had a significantly higher mean FMD than the group with higher excretion, despite similar age, BMI, mean BP, medication use, and aldosterone excretion. For five subjects with very low sodium excretion, FMD was even better, suggesting a dose-response relationship between sodium excretion and endothelial function.
Association of brachial-artery flow-mediated dilation and urinary sodium excretion in subjects with aldosteronism and resistant hypertension
|
End point |
Low (<150 meq/24 hr), n=10 |
High (>150 meq/24 hr), n=24 |
Very low (< 100 meq/24 hr), n=5 |
|
Mean FMD (%) | 2.6 + 1.0 | 1.6 + 1.0* | 3.4 + 0.7 |
Aldosterone antagonists eplerenone and spironolactone are already in use for patients with heart failure, but there have not to date been any studies of these agents in patients with hypertension, Calhoun added. "We're suggesting that aldosterone is an independent cardiovascular risk factor based on our study, so we would predict that aldosterone antagonists in these high-risk patients would provide cardiovascular benefit beyond BP reduction," he said. "We'd like to see that tested."
