The two mechanisms involved in the control of urinary kallikrein excretion

The relation between sodium and kallikrein excretion is biphasic. Increased kallikrein excretion is produced by increased arterial pressure or arterial infusion of vasodilators. It is antagonised by prostaglandin synthesis inhibition or by arterial noradrenaline infusion. Angiotensin in hypertensive doses increases kallikrein excretion and this effect is pressure dependent. Decreasing sodium intake, or producing natriuresis with diuretics, causes a rise in kallikrein excretion by stimulation of the renin/angiotensin/prostaglandin/kallikrein chain. It can be mimicked by infusing 50 micrograms/min of angiotensin II into one renal artery with a clamp to prevent elevation of renal arterial pressure.