Control of renin synthesis and secretion

Abstract

The aspartyl protease renin is the rate limiting activity of the renin-angiotensin-aldosterone system (RAAS). Renin is synthesized as an enzymatically inactive proenzyme which is constitutively secreted from several tissues. Only renin-expressing cells in the kidney are capable of generating active renin from prorenin, which is stored in prominent vesicles and which is released into the circulation upon demand. The acute release of renin is controlled by cyclic adenosine monophosphate (cAMP) and by calcium signaling pathways, which in turn are activated by a number of systemic and local factors. Longer lasting challenges of renin secretion lead to changes in the number of renin-producing cells, which occur by a metaplastic transformation of renin cell precursors such as preglomerular vascular smooth muscle or extraglomerular mesangial cells. This review aims to briefly address the state of knowledge of these various aspects of renin synthesis and secretion and attempts to relate them to the in vivo situation, in particular in men.