Renin is a zinc-containing enzyme with 340 amino acids of molecular mass ~37 kDa. Renin can be isolated from both human and rat kidneys and mouse submaxillary glands. The original isolation of the pure protein required a 3 million-fold purification; the primary sequence of human renin has been deduced through cloning and sequence analysis of cDNA prepared from human kidney mRNA. Renin as an enzyme belongs to the class of aspartyl proteinases.

Renin is biosynthesized as a prepro-renin consisting of 406 amino acids. The prepro form is converted to prorenin by the removal of the first 20 amino acids of the pre-segment followed by the removal of a pro-segment of 46 amino acids. Approximately 50% of the prorenin in the juxtaglomerular cells is constitutively secreted continuously without proteolytic processing, while the other 50% of the prorenin is sorted to secretory granules, where it is proteolytically processed and stored as renin. The release of this renin is regulated by cAMP. Renin in the circulatory system is variably glycosylated and circulates as 4–5 isoenzymes.

In renin, the aspartyl residues at positions 38 and 226 are believed to be important for catalytic activity. The X-ray crystallographic structure of human renin has been determined to the 2.5 Å level. The general shape of renin is bilobal with a long deep cleft that contains the aspartyl 38 and 226 residues.

Changes in the secretion of renin by the renal juxtaglomerular cells can occur in response to changes in renal arterial pressure, via sympathetic nervous system signals and also via changes in the status of a number of hormones (see Table 1). The secretion of renin is governed at the level of the renal glomerulus by both long and short feedback loops. The dominant negative long feedback loop, which diminishes renin secretion, occurs when there is an increased renal arterial pressure, which is sensed by stretch receptors present in the glomerular afferent arteriolar wall so as to result in a reduction in renin release and, ultimately, a diminution in aldosterone production. A negative short feed back loop is mediated by angiotensin II, which directly inhibits renin release.

Table1. Factors Regulating Renin Release

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مواضيع ذات صلة

Nephron Function in Chronic Kidney Disease

Injury to The Renal Vasculature as A Cause OF Chronic Kidney Disease

Vicious Cycle of Chronic Kidney Disease Leading to End-Stage Renal Disease

Intrarenal Acute Kidney Injury Caused by Abnormalities Within the Kidney

Prerenal Acute Kidney Injury Caused by Decreased Blood Flow to the Kidney

kidney Diseases

Diuretics and Their Mechanisms of Action

Conditions That Cause Large Increases in Extracellular Fluid Volume but with Normal Blood Volume

Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume

Integrated Responses to Changes in Sodium Intake

Role of Atrial Natriuretic Peptide in Controlling Renal Excretion

Role of Aldosterone in Controlling Renal Excretion