The role of renin in the control of the circulation and in hypertensive disease

Renin is a hormone secreted by the juxtaglomerular cells of the kidney; it interacts with a plasma protein substrate to produce a decapeptide prohormone angiotensin I. Converting hormone located on vascular endothelium converts the decapeptide to an octapeptide, angiotensin II, which effects vasoconstriction, the secretion of aldosterone by the adrenal cortex, and retention of sodium by the kidney. The biosynthesis and control of Renin secretion are not well understood, and the question as to whether Renin is synthesized and stored in a larger precursor form is as yet unresolved. Whether or not higher molecular weight or inactive forms of Renin in plasma have a role in controlling Renin activity or whether they simply represent a degradative pathway for Renin is as yet uncertain. The availability of several inhibitors of the renin-angiotensin system has served to define the role of Renin both in normal cardiovascular homeostasis and in renovascular hypertension. It appears that Renin plays an important role in maintaining blood pressure in the salt- or volume-depleted state and that it is responsible for the initial phases of renovascular hypertension in any model of this disease process. Renin's part in chronic renovascular hypertension depends on whether or not sodium is permitted to accumulate. If sodium intake is restricted or if sodium excretion is unimpaired (such as in two-kidney renovascular hypertension models), Renin continues to play a significant role during the chronic phase.