Why is renin released from the kidneys

The macula densa senses the concentration of sodium and chloride ions in the tubular fluid. When NaCl is elevated in the tubular fluid, renin release is inhibited. In contrast, a reduction in tubular NaCl stimulates renin release by the JG cells. When afferent arteriole pressure is reduced, glomerular filtration decreases, and this reduces NaCl in the distal tubule. This serves as an important mechanism contributing to the release of renin when there is afferent arteriole hypotension, which can be caused by systemic hypotension or narrowing stenosis of the renal artery that supplies blood flow to the kidney.

When renin is released into the blood, it acts upon a circulating substrate, angiotensinogen , that undergoes proteolytic cleavage to form the decapeptide angiotensin I. Vascular endothelium, particularly in the lungs, has an enzyme, angiotensin converting enzyme ACE , that cleaves off two amino acids to form the octapeptide, angiotensin II AII , although many other tissues in the body heart, brain, vascular also can form AII.

The renin-angiotensin-aldosterone pathway is not only regulated by the mechanisms that stimulate renin release, but it is also modulated by natriuretic peptides released by the heart.

These natriuretic peptides acts as an important counter-regulatory system. Therapeutic manipulation of this pathway is very important in treating hypertension and heart failure. ACE inhibitors , AII receptor blockers and aldosterone receptor blockers , for example, are used to decrease arterial pressure, ventricular afterload, blood volume and hence ventricular preload, as well as inhibit and reverse cardiac and vascular hypertrophy. Cardiovascular Physiology Concepts Richard E.

Klabunde, PhD. In the adult organism, systemically circulating renin almost exclusively originates from the juxtaglomerular cells in the afferent arterioles of the kidneys. These cells share similarities with pericytes and myofibro-blasts. They store renin in a vesicular network and granules and release it in a regulated fashion. The release mode of renin is not understood; in particular, the involvement of SNARE proteins is unknown. Renin release is acutely increased via the cAMP signaling pathway, which is triggered mainly by catecholamines and other G s -coupled agonists, and is inhibited by calcium-related pathways that are commonly activated by vasoconstrictors.