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Renin (etymology and pronunciation), also known as an angiotensinogenase, is an aspartic protease protein and enzyme secreted by the kidneys that participates in the body's renin-angiotensin-aldosterone system (RAAS)—also known as the renin-angiotensin-aldosterone axis—that increases the volume of extracellular fluid (blood plasma, lymph, and interstitial fluid) and causes arterial ...
Locally expressed renin–angiotensin systems have been found in a number of tissues, including the kidneys, adrenal glands, the heart, vasculature and nervous system, and have a variety of functions, including local cardiovascular regulation, in association or independently of the systemic renin–angiotensin system, as well as non ...
This mechanism, which runs from renin through Ang II and to aldosterone, as well as the negative feedback that Ang II has on renin secretion, is known as RAAS. [23] The net effect is to increase blood pressure, which in normal physiology is necessary in order to maintain homeostasis.
Juxtaglomerular cells secrete renin in response to a drop in pressure detected by stretch receptors in the vascular walls, or when stimulated by macula densa cells. Macula densa cells are located in the distal convoluted tubule, and stimulate juxtaglomerular cells to release renin when they detect a drop in chloride concentration in tubular fluid.
Excess secretion of renin by the juxtaglomerular cells can lead to excess activity of the renin–angiotensin system, hypertension and an increase in blood volume. This is not responsive to the usual treatment for essential hypertension, namely medications and lifestyle modification.
This, and similar findings obtained in vivo, [15] has led some to believe that perhaps "the initiating signal for MD control of renin secretion is a change in the rate of NaCl uptake predominantly via a luminal Na,K,2Cl co-transporter whose physiological activity is determined by a change in luminal Cl concentration." [16]
Renin is the first in a series of important chemical messengers that make up the renin–angiotensin system. Changes in renin ultimately alter the output of this system, principally the hormones angiotensin II and aldosterone .
Schematic diagram of the renin–angiotensin–aldosterone system Angiotensin II is a potent vasoconstrictor in a substrate concentration-dependent manner. [ 10 ] Angiotensin II binds to the type 1 angiotensin II receptor (AT1) , which sets off a number of actions that result in vasoconstriction and therefore increased blood pressure.