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Renin (/ˈriːnɨn/ ree-nin), also known as an angiotensinogenase, is an enzyme that participates in the body's renin-angiotensin system (RAS)—also known as the renin-angiotensin-aldosterone axis—that mediates extracellular volume (i.e., that of the blood plasma, lymph and interstitial fluid), and arterial vasoconstriction. Thus, it regulates the body's mean arterial blood pressure.

Renin is often improperly referred to as a hormone even though it has no peripheral receptors and rather has an enzymatic activity with which it hydrolyses angiotensinogen to angiotensin I.

Secretion

The enzyme renin is secreted by the afferent arterioles of the kidney from specialized cells called granular cells of the juxtaglomerular apparatus in response to three stimuli:

1-A decrease in arterial blood pressure (that could be related to a decrease in blood volume) as detected by baroreceptors (pressure-sensitive cells). This is the most direct causal link between blood pressure and renin secretion (the other two methods operate via longer pathways).

2-A decrease in sodium chloride levels in the ultrafiltrate of the nephron. This flow is measured by the macula densa of the juxtaglomerular apparatus.

3-Sympathetic nervous system activity, which also controls blood pressure, acting through the beta1 adrenergic receptors.

Human renin is secreted by at least 2 cellular pathways: a constitutive pathway for the secretion of prorenin and a regulated pathway for the secretion of mature renin

Renin activates the renin-angiotensin system by cleaving angiotensinogen, produced by the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE, the angiotensin-converting enzyme primarily within the capillaries of the lungs. Angiotensin II then constricts blood vessels, increases the secretion of ADH and aldosterone, and stimulates the hypothalamus to activate the thirst reflex, each leading to an increase in blood pressure. Renin's primary function is therefore to eventually cause an increase in blood pressure, leading to restoration of perfusion pressure in the kidneys.

Renin is secreted from juxtaglomerular kidney cells, which sense changes in renal perfusion pressure, via stretch receptors in the vascular walls. The juxtaglomerular cells are also stimulated to release renin by signaling from the macula densa. The macula densa sense changes in volume delivery to the distal tubule, and responds to a drop in tubular volume by stimulating renin release in the juxtaglomerular cells. Together, the macula densa and juxtaglomerular cells comprise the juxtaglomerular complex.

Renin secretion is also stimulated by sympathetic nervous stimulation, mainly through beta-1 adrenoceptor activation.

References .

1-Imai, T.; Miyazaki, H.; Hirose, S.; Hori, H.; Hayashi, T.; Kageyama, R.; Ohkubo, H.; Nakanishi, S.; and Murakami, K. (December 1983). "Cloning and sequence analysis of cDNA for human renin precursor". Proceedings of the National Academy of Sciences U.S.A. 80 (24): 7405–9.

2-Jump up ^ Pratt, R. E.; Flynn, J. A.; Hobart, P. M.; Paul, M.; and Dzau, V. J. (March 1988). "Different secretory pathways of renin from mouse cells transfected with the human renin gene". Journal of Biological Chemistry 263 (7): 3137–41.

3-Jump up ^ Page 866-867 (Integration of Salt and Water Balance) and 1059 (The Adrenal Gland) in:Boulpaep, E. L.; and Boron, W. F. (2005). Medical physiology: a cellular and molecular approach. St. Louis, MO: Elsevier Saunders. ISBN 1-4160-2328-3.

4-Jump up ^ Fujino, T.; Nakagawa, N.; Yuhki, K.; Hara, A.; Yamada, T.; Takayama, K.; Kuriyama, S.; Hosoki, Y.; Takahata, O.; Taniguchi, T.; Fukuzawa, J.; Hasebe, N.; Kikuchi, K.; Narumiya, S.; and Ushikubi, F. (September 2004). "Decreased susceptibility to renovascular hypertension in mice lacking the prostaglandin I2 receptor IP". Journal of Clinical Investigation 114 (6): 805–12.

5-Jump up ^ Brenner & Rector's The Kidney, 7th ed., Saunders, 2004, pp. 2118-2119.

6-Jump up ^ Hamilton Regional Laboratory Medicine Program - Laboratory Reference Centre Manual. [deadlink]

7-Jump up ^ Nguyen, Geneviève; Delarue, Françoise; Burcklé, Céline; Bouzhir, Latifa; Giller, Thomas; and Sraer, Jean-Daniel (June 2002). "Pivotal role of the renin/prorenin receptor in angiotensin II production and cellular responses to renin". Journal of Clinical Investigation 109 (11): 1417–27.

Good luck

Hello, Brother Saleh Alkarim,

very good answer from you, thank you very much for this.

i still have the main question, which is: what is the main reason of high blood pressure? is it the secretion of angiotensinogen from liver? or the action of ACE?.

to be very clearly, all of us have these secretions, why it cause high blood pressure for some one? and does not give the same action for others.

Dear Ebrahim sir

ACE is one of the main reason of leading to the hypertension, so many research article are available which give a clear idea about the ACE and its inhibitor and thier mechanism of action.

Dear Saleh Alkarim

Thank you so much for giving the valuable information

with regards

Mithun V. K. Patil

Daeprtment of Pharmacology

Poona college of Pharmacy,

B.V.D.U

Pune, India

Liver angiotensinogen synthesis and release during captopril treatment in sodium-depleted rats.

Jaramillo HN, Sambhi MP, Bouhnik J, Corvol P, Menard J.

Abstract

In vivo generation of angiotensins depends upon both plasma renin and angiotensinogen concentrations. Those factors which may influence hepatic angiotensinogen synthesis and release were examined. We have evaluated in vivo the effects of converting enzyme inhibition on several plasma renin-angiotensin system components, and, using an in vitro preparation of liver slices, we also investigated the effects of converting enzyme inhibition on the synthesis and release of hepatic angiotensinogen. Angiotensinogen concentrations were determined by two different methods. The first was an indirect enzymatic assay which measures the amount of angiotensin I liberated from plasma by an excess of renin. The second was a direct RIA that measures both angiotensinogen and its inactive residue the des-angiotensin I-angiotensinogen. The difference between the methods represents the circulating levels of des-angiotensin I-angiotensinogen. Captopril administration in sodium-depleted rats increased plasma concentrations of renin, des-angiotensin I-angiotensinogen, and angiotensin I and decreased plasma angiotensinogen concentration measured by both methods. Plasma des-angiotensin I-angiotensinogen was significantly correlated to plasma renin concentration, which suggests an increase in the consumption of angiotensinogen when the renin secretion is extremely increased. The angiotensinogen liver content and in vitro angiotensinogen release were decreased in sodium-depleted rats treated with a converting enzyme inhibitor, and these parameters were negatively correlated to in vivo plasma levels of renin, angiotensin I, and des-angiotensin I-angiotensinogen. They were positively correlated to plasma angiotensinogen concentration measured by the indirect assay. These data suggest that captopril administration during sodium depletion has two simultaneous effects: it increases angiotensinogen consumption and second, decreases angiotensinogen production and release.

Thank you very much Mithun Vishwanath K. Patil and Mohammadreza Seyyedmajidi for your kind reply

Glucocorticoids and oestrogen increase angiotensinogen secretion from the liver. Oestrogen do this somewhat more in the females than in the males. Besides this, the effect of oestrogens is greater in the presence of prolactin or shall I say requires the presence of prolactin. Renin inhibits liver angiotensin secretion.