Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism

Urinary kallikrein excretion was measured before and after administration of spironolactone in 12 patients with essential hypertension (including 7 patients with low renin and 5 patients with normal renin) and 6 patients with primary aldosteronism. In low renin essential hypertension, two types of urinary kallikrein excretion were observed. In one type, urinary kallikrein decreased from 6.2+/-2.1 (S.E.) EU/day to 2.7+/-0.3 EU/day after the treatment. In another type, urinary kallikrein increased from 3.1+/-0.5 EU/day to 6.4+/-1.0 EU/day. In the former, plasma aldosteron showed high levels (12.3+/-2.1 ng/100 ml), while in the latter, it was normal (3.2+/-0.5 ng/100 ml). In normal renin essential hypertension, urinary kallikrein excretion did not alter after the treatment. In primary aldosteronism, urinary kallikrein showed moderate decrease after the spironolactone treatment from 8.5+/-1.6 EU/day to 4.2+/-1.6 EU/day. Spironolactone is said to compete directly with the effect of aldosterone at renal distal tubules. The present investigation suggests that urinary kalikrein excretion is related to the effective levels of aldosterone at renal distal tubules, and alteration of aldosterone levels mediates the release of kallikrein, and that there are different mechanisms in the renal handling of sodium and kallikrein in low renin essential hypertension, in normal renin essential hypertension, and in primary aldosteronism.