"Renin: The activity of these systems depends on the level of renin gene expression and on conversion of prorenin to active renin by proteolytic removal of a 43 amino acid prosegment. Renin is stored in secretory granules of the juxtaglomerular cells of the kidney and is released in response to various physiological stimuli, such as low blood pressure blockade of Ang II production or decreases in distal tubular sodium. It is an enzyme that triggers the cascade by cleaving the liver-derived angiotensinogen into angiotensin I (Ang I).
The major determinant of renin secretion is sodium intake; low intake or fluid loss lowers the extracellular volume and stimulates renin secretion. There are three mechanisms regulating renin release. The first is through afferent arteriolar baroreceptors; in response to low arterial perfusion pressure renin release increases. The second is through sympathetic innervation of the juxtaglomerular cells, stimulation of these neurons leads to norepinephrine release and subsequent stimulation of beta1-adrenergic receptors stimulating renin release. The third is a negative feedback mechanism through binding of Ang II to AT1 and AT2 receptors.
(An-Sofie Goessaert, Johan Vande Walle, Ayush Kapila and Karel Everaert- Hormones and Nocturia: Guidelines for Medical Treatment?)
Last date updated on June, 2014