Aldosterone and renin measurements

Renin (EC 3.4.99.19) is an aspartyl protease glycoprotein with a molecular weight of approximately 30 000±40 000. It catalyses the cleavage of a decapeptide, angiotensin I, from the circulating substrate, angiotensinogen (Fig. 1). Angiotensin I is further converted to an octapeptide, angiotensin II, by the action of angiotensin-converting enzyme (ACE). Angiotensin II is a powerful vasoconstrictor, acting on the arterioles. It is also the predominant regulator of aldosterone synthesis and secretion. Aldosterone is the major mineralocorticoid secreted by the adrenal cortex. It acts on the distal renal tubule and also on the gut to promote the reabsorption of sodium and the secretion of potassium and hydrogen ions. Thus, the renin±angiotensin±aldosterone system plays a central role in the regulation of arterial blood pressure and in the maintenance of sodium and potassium homeostasis. Renin is found in the circulation in two forms. The form that catalyses the production of angiotensin I is sometimes referred to as `active renin’, but is often called `plasma renin activity’ or just simply `renin’. The other form of renin found in plasma does not catalyse the production of angiotensin I, and is known as `prorenin’. Although prorenin can be converted to active renin by proteolytic action, this process is not believed to occur in vivo. Renin is released from the renal juxtaglomerular cells in an active form in response to various physiological factors, the most important being sodium depletion, decreased blood volume and pressure and badrenergic stimulation. Whenever the systemic blood pressure falls, the rate of renin release increases (due to activation of the renal baroreceptor and the sympathetic nervous system). The increase in circulating renin leads to an increase in the rate of angiotensin II formation. This promotes arteriolar vasoconstriction and maintenance of blood pressure, and, via the action of aldosterone, the increased reabsorption of sodium by the kidney. Although the renin±angiotensin±aldosterone axis is often discussed in isolation, it interacts with several other humoral and local factors which are discussed in detail in recent reviews.