Human urinary and plasma kinins: relationship to sodium-retaining steroids and plasma renin activity.

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Abstract
Na-retaining steroids increase urinary kallikrein but their effects on urinary kinins and plasma bradykinin are not known. Normal subjects (36) were studied during several different manipulations of dietary Na and K or the administration of fludrocortisone or ACTH. Urinary kallikrein and aldosterone excretion changed pari passu over a 30-fold range for kallikrein and an 80-fold range for aldosterone. Urinary kinin excretion was invariant. Plasma bradykinin responded to the same stimuli as plasma renin activity and not primarily to the level of Na-retaining steroid. Urinary kallikrein was dependent on the level of aldosterone over a wide range of excretion values. Urinary kallikrein determined neither the level of urinary kinins nor the level of plasma kinins. Urinary kinins were independent of the level of Na-retaining steroid. There was a strong correlation between plasma bradykinin and renin activity but not between plasma bradykinin and Na-retaining steroid activity. Urinary kallikrein is apparently an index of Na-retaining steroid activity and may participate in the antinatriuretic and kaliuretic effects of these hormones. Plasma bradykinin is apparently highly correlated with plasma renin activity because both responded to changes in extracellular fluid volume and not because angiotensin-converting enzyme controls both systems in an interrelated fashion. Plasma bradykinin may act physiologically to antagonize angiotensin II and may contribute to maintenance of normal blood pressure in hyperreninemic states.