1. Excretion of urinary kallikrein was normal in 13 out of 15 patients with uncomplicated essential hypertension.

2. Frusemide increased urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension. The stimulating effect of frusemide on urinary kallikrein was significantly diminished in patients with essential hypertension.

3. No correlations of urinary kallikrein with sodium, potassium, and aldosterone excretion were found.

4. The results do not support the idea that urinary kallikrein plays a primary role in the pathogenesis of essential hypertension.

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