The Biochemistry of the Renin-Angiotensin System

Lt, Skeggs; Fe, Dorer; Levine, Martin; Ke, Lentz; Kahn, Jeffrey D.

doi:10.1007/978-1-4615-9173-3_1

Cited by 91 publications

(89 citation statements)

References 84 publications

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“…7 ACE is anchored to the plasma membrane through a single carboxyterminal transmembrane domain and, at the cell surface, ACE functions as an ectoenzyme that hydrolyzes circulating peptides. ACE may be cleaved from the cell surface and act as a soluble enzyme, but the biological significance of soluble ACE remains unclear.…”

Section: Ace2 a New Member Of The Rasmentioning

confidence: 99%

Angiotensin-Converting Enzyme 2 (ACE2) in Disease Pathogenesis

Imai

Kuba

Ohto-Nakanishi

et al. 2010

Circ J

180

164

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Angiotensin-converting enzyme 2 (ACE2), a first homolog of ACE, regulates the renin-angiotensin system by counterbalancing ACE activity. Accumulating evidence in recent years has demonstrated a physiological and pathological role of ACE2 in the cardiovascular, renal and respiratory systems. For instance, in the acute respiratory distress syndrome (ARDS), ACE, AngII, and AT1R promote the disease pathogenesis, whereas ACE2 and the AT2R protect from ARDS. Importantly, ACE2 has been identified as a key SARS-coronavirus receptor and plays a protective role in SARS pathogenesis. Furthermore, the recent explosion of research into the ACE2 homolog, collectrin, has revealed a new physiological function of ACE2 as an amino acid transporter, which explains the pathogenic role of gene mutations in Hartnup disorder. This review summarizes and discusses the recently unveiled roles for ACE2 in disease pathogenesis. (Circ J 2010; 74: 405 - 410)

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Section: Ace2 a New Member Of The Rasmentioning

confidence: 99%

Angiotensin-Converting Enzyme 2 (ACE2) in Disease Pathogenesis

Imai

Kuba

Ohto-Nakanishi

et al. 2010

Circ J

180

164

View full text Add to dashboard Cite

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“…The main effector of the RAS is the key component angiotensin (Ang) II that mediates the majority of its cardiac and renal actions by binding Ang II type 1 receptor (AT1R). 51,52 Responses include vascular smooth muscle contraction, enhanced myocardial contractility, aldosterone secretion, catecholamine release from medulla and sympathetic nerve endings, adrenergic stimulation, increased sympathetic nervous system activity, renal sodium reabsorption and thirst and salt appetite stimulation. 53,54 Ang II also binds to Ang II type 2 receptor (AT2R), inducing a counter regulatory vasodilation through the stimulation of (NO)/cGMP, mediated by bradykinin release (aorta, heart, kidney), but also growth inhibition and apoptosis promotion.…”

Section: Ntt4 (Slc6a17)mentioning

confidence: 99%

Collectrin and ACE2 in renal and intestinal amino acid transport

Singer¹,

Camargo²

2011

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Neutral amino acid transporters of the SLC6 family are expressed at the apical membrane of kidney and/or small intestine, where they (re-)absorb amino acids into the body. In this review we present the results concerning the dependence of their apical expression on their association to partner proteins. We will in particular focus on the situation of B(0)AT1 and B(0)AT3, which associate with members of the renin-angiotensin system (RAS), namely Tmem27 and angiotensin-converting enzyme 2 (ACE2), in a tissue specific manner. The role of this association in relation to the formation of a functional unit related to Na(+) or amino acid transport will be assessed. We will conclude with some remarks concerning the relevance of this association to Hartnup disorder, where some mutations have been shown to differentially interact with the partner proteins

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“…It has been known for years that the kidney releases renin into the general circulation where it acts upon a microglobulin (103,157) from which several active peptides are produced, ANG II being the one that exerts the most prominent pressor effect (21,128). ANG II can also be generated by renin within the kidney.…”

Section: Circulating and Intrarenal Levels Of Ang IImentioning

confidence: 99%

Role of oxidative stress in angiotensin-induced hypertension

Reckelhoff

Romero

2003

American Journal of Physiology-Regulatory, Integrative and Comp

167

133

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Reckelhoff, Jane F., and J. Carlos Romero. Role of oxidative stress in angiotensin-induced hypertension. Am J Physiol Regul Integr Comp Physiol 284: R893-R912, 2003; 10.1152/ajpregu.00491.2002.-Infusion of ANG II at a rate not sufficient to evoke an immediate vasoconstrictor response, produces a slow increase in blood pressure. Circulating levels of ANG II may be within ranges found in normotensive individuals, although inappropriately high with respect to sodium intake. When ANG II levels are dissociated from sodium levels, oxidative stress (OXST) occurs, which can increase blood pressure by several mechanisms. These include inadequate production or reduction of bioavailability of nitric oxide, alterations in metabolism of arachidonic acid, resulting in an increase in vasoconstrictors and decrease in vasodilators, and upregulation of endothelin. This cascade of events appears to be linked, because ANG II hypertension can be blocked by inhibition of any factor located distally, blockade of ANG II, OXST, or endothelin. Such characteristics are shared by other models of hypertension, such as essential hypertension, hypertension induced by reduction in renal mass, and renovascular hypertension. Thus these findings are clinically important because they reveal 1) uncoupling between ANG II and sodium, which can trigger pathological conditions; 2) the various OXST mechanisms that may be involved in hypertension; and 3) therapeutic interventions for hypertension developed with the knowledge of the cascade involving OXST.isoprostanes; endothelin; spontaneous hypertension; renovascular hypertension; sodium balance THREE DECADES AGO, the production of free radicals was thought to be the result of severe injuries or pathological insults such as those resulting from exposure to high-energy radiation or toxins such as carbon tetrachloride (127). However, in 1968, the discovery of superoxide dismutase (SOD) by McCord and Fridovich (96) strongly suggested that all aerobically metabolizing cells are capable of producing superoxide ions, which could play a role in normal metabolic processes. The concomitant discovery of the biology of nitric oxide (NO) strongly suggested that free radicals could constitute the basis of metabolic regulation (67,90,118). One of the first findings supporting such a notion was the demonstration that the inhibition of the synthesis of NO produced by the administration of an NO synthesis competitor, such as N -monomethyl-Larginine] or N G -nitro-L-arginine methyl ester (L-NAME), produced a marked vasoconstriction (13,136,173), sodium retention (82, 83), and thereby a sustained increase in mean arterial pressure (MAP) (13,82,83,136,173). The identification of a specific pathological situation in humans, where a decrease of NO may end up in an elevation of blood pressure was thought to be linked to endothelial dysfunction (105), such as those involved in aging, arteriosclerosis, etc., but the specific metabolic alterations involved in this process were poorly understood. However, the relationship betw...

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The Biochemistry of the Renin-Angiotensin System

Cited by 91 publications

References 84 publications

Angiotensin-Converting Enzyme 2 (ACE2) in Disease Pathogenesis

Angiotensin-Converting Enzyme 2 (ACE2) in Disease Pathogenesis

Collectrin and ACE2 in renal and intestinal amino acid transport

Role of oxidative stress in angiotensin-induced hypertension

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