Key result
Spironolactone lowers urinary prostasin in normotensives, but levels paradoxically rise with volume expansion in aldosteronism.
Why the study?
The potential of urinary prostasin as a candidate marker of ENaC activation in humans was investigated due to its hypothesized regulatory role in animals and in vitro.
Does spironolactone or saline/Florinef alter urinary prostasin levels in healthy volunteers and hypertensive patients?
Does spironolactone or saline/Florinef alter urinary prostasin levels in healthy volunteers and hypertensive patients?
Urinary prostasin contains an aldosterone-responsive fraction modulated by sodium intake, making it a potential candidate marker for ENaC activation in humans.
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Differential prostasin responses to spironolactone may distinguish hypertension subtypes; hypothesis-generating for biomarker validation.
Olivieri et al. (2005) studied Primary aldosteronism (n=18). Spironolactone or saline/Florinef suppression test vs. Baseline (before intervention) was evaluated on Urinary prostasin levels. Spironolactone (100 mg) decreased urinary prostasin in normotensives on low sodium intake, whereas prostasin paradoxically increased in primary aldosteronism patients after volume expansion.
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