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

Sodium-retaining steroids increase urinary kallikrein but their effects on urinary kinins and plasma bradykinin are not known. Thirty-six normal subjects were studied during several different manipulations of dietary sodium and potassium or the administration of fludrocortisone or adrenocorticotropic hormone (ACTH). Urinary kallikrein and aldosterone excreting changed pari passu over a 30-fold range for kallikrein and an 80-fold range for aldosterone. Urinary kinin excretion was invariant. Plasma, bradykinin, on the other hand, responded to the same stimuli as plasma renin activity and not primarily to the level of sodium-retaining steroid. These studies show that: urinary kallikrein is dependent on the level of aldosterone over a wide range of excretion values; urinary kallikrein determines neither the level of urinary kinins nor the level of plasma kinins; urinary kinins are independent of the level of sodium-retaining steroid; and there is a strong correlation between plasma bradykinin and renin activity but not between plasma bradykinin and sodium-retaining steroid activity. We suggested that: urinary kallikrein is an index of sodium-retaining steroid activity and may participate in the antinatriuretic and kaliuretic effects of these hormones; plasma bradykinin is 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; and plasma bradykinin may act physiologically to antagonize angiotensin II and may contribute to maintenance of normal blood pressure in hyperreninemic states.