Background: A continuum of non-suppressible aldosterone production has been demonstrated in normotensive individuals, termed subclinical primary aldosteronism (PA), and is consistently associated with increased risk for developing hypertension and cardiovascular disease. The hormonal mechanisms accounting for subclinical PA are not well understood.
Method: To quantify the magnitude of subclinical PA, prospectively recruited normotensive participants (n=75) had their maximally suppressed plasma aldosterone assessed after maintaining supine posture following an oral sodium loading protocol.