ACE2–angiotensin-(1–7)–Mas axis in renal ischaemia/reperfusion injury in rats

Silveira, Kátia D.; Bosco, Kênia S. Pompermayer; Diniz, Lúcio Ricardo Leite; Carmona, Adriana K.; Cassali, G. D.; Bruna-Romero, Oscar; Sousa, Lirlândia P.; Teixeira, Mauro Martins; Santos, Robson A.S.; Silva, Ana Cristina Simões e; Vieira, Maria Aparecida Ribeiro

doi:10.1042/cs20090554

Cited by 98 publications

(110 citation statements)

References 41 publications

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“…The data in that study also showed that the biphasic effect of ANG-(1-7) on the Na+/H+ exchanger occurred via the Mas receptor and that A779 (a Mas receptor antagonist) abolished this hormonal biphasic effect. These results are also consistent with previously described findings in the literature that indicated that the renal effects of ANG-(1-7) are dose dependent and mediated, at least in part, by the Mas receptor [193][194][195][196]. Nevertheless, in isolated rat proximal straight tubules (S3 segment), it was shown that, like ANG II, ANG-(1-7) exerts a biphasic effect through AT1 receptors: at physiological levels, ANG-(1-7) increases fluid and bicarbonate reabsorption, while at high concentrations, ANG-(1-7) decreases these parameters [183].…”

Section: Actions Of Ang-(1-7) In the Kidneysupporting

confidence: 82%

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

Mello-Aires¹,

Dellova²,

Castelo‐Branco³

et al. 2017

Nephrol Renal Dis

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This article reviews the main body of knowledge regarding NHE1 and NHE3 exchangers and their interaction with Angiotensin II, Angiotensin-(1-7), Aldosterone and Arginine Vasopressin, particularly their renal actions. This work addresses the biphasic effects of different hormonal doses on NHE1 or NHE3 in proximal tubule in Wistar, SHR (hypertensives) and their control WKY (normotensives) rats or MDCK cells (which share similarities with the collecting duct). The hormones were applied alone, with their inhibitors or plus agents that change the [Ca 2+ ]i. The data are compatible with hormonal stimulation of these exchangers by increases of [Ca 2+ ]i in lower range, and inhibition at high [Ca 2+ ]i. In MDCK cells and Wistar rats, low doses of ANG II, ALDO or AVP stimulated the exchangers, while high doses inhibited them. ANG-(1-7), in Wistar or WKY rats has inverse, dose-dependent effects. In SHR rats, the biphasic effects of ANG-(1-7) were similar to the effects of ANG II, ALDO or AVP in Wistar rats. The interactions between these effects may represent a mechanism that regulates extracellular volume. In hypertensives animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated hypertension. Figure 6 shows a schematic model to describe these biphasic hormonal effects.

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Section: Actions Of Ang-(1-7) In the Kidneysupporting

confidence: 82%

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

Mello-Aires¹,

Dellova²,

Castelo‐Branco³

et al. 2017

Nephrol Renal Dis

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“…Angiotensin II increases and angiotensin 1-7 decreases in kidney tissue after ischemia reperfusion injury in rats (28,29). Interestingly, intrarenal angiotensin II concentration strongly correlates with urinary angiotensinogen concentration but is not correlated with plasma angiotensinogen, which implies that elevated urinary angiotensinogen reflects activation of the intrarenal RAS (30).…”

Section: Discussionmentioning

confidence: 80%

Association of Elevated Urinary Concentration of Renin-Angiotensin System Components and Severe AKI

Alge

Karakala

Neely

et al. 2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground Prognostic biomarkers that predict the severity of AKI at an early time point are needed. Urinary angiotensinogen was recently identified as a prognostic AKI biomarker. The study hypothesis is that urinary renin could also predict AKI severity and that in combination angiotensinogen and renin would be a strong predictor of prognosis at the time of AKI diagnosis.Design, setting, participants, & measurements In this multicenter, retrospective cohort study, urine was obtained from 204 patients who developed AKI after cardiac surgery from August 2008 to June 1, 2012. All patients were classified as having Acute Kidney Injury Network (AKIN) stage 1 disease by serum creatinine criteria at the time of sample collection. Urine output was not used for staging. Urinary angiotensinogen and renin were measured, and the area under the receiver-operating characteristic curve (AUC) was used to test for prediction of progression to AKIN stage 3 or in-hospital 30-day mortality. These biomarkers were added stepwise to a clinical model, and improvement in prognostic predictive performance was evaluated by category free net reclassification improvement (cfNRI) and chi-squared automatic interaction detection (CHAID).Results Both the urinary angiotensinogen-to-creatinine ratio (uAnCR; AUC, 0.75; 95% confidence interval [CI], 0.65 to 0.85) and the urinary renin-to-creatinine ratio (uRenCR; AUC, 0.70; 95% CI, 0.57 to 0.83) predicted AKIN stage 3 or death. Addition of uAnCR to a clinical model substantially improved prediction of the outcome (AUC, 0.85; cfNRI, 0.673), augmenting sensitivity and specificity. Further addition of uRenCR increased the sensitivity of the model (cfNRI events , 0.44). CHAID produced a highly accurate model (AUC, 0.91) and identified the combination of uAnCR .337.89 ng/mg and uRenCR .893.41 pg/mg as the strongest predictors (positive predictive value, 80.4%; negative predictive value, 90.7%; accuracy, 90.2%). ConclusionThe combination of urinary angiotensinogen and renin predicts progression to very severe disease in patients with early AKI after cardiac surgery.

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“…Alenina et al (2008) reported that Mas mRNA is predominantly found in the renal cortex of male mice. Indeed, functional Mas is detected in proximal tubules, as well as in the afferent arterioles, collecting ducts and the thick ascending limb of Henle and its expression is upregulated in renal ischemia (Ren et al 2002, Gwathmey et al 2010, Silveira et al 2010, Zimmerman & Burns 2012.…”

Section: Vascular Actions Of the Ace2/ang-(1-7)/mas Axismentioning

confidence: 99%

Angiotensin-converting enzyme 2, angiotensin-(1–7) and Mas: new players of the renin–angiotensin system

Santos

Ferreira

Verano‐Braga

et al. 2012

Journal of Endocrinology

439

369

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Angiotensin (Ang)-(1-7) is now recognized as a biologically active component of the reninangiotensin system (RAS). Ang-(1-7) appears to play a central role in the RAS because it exerts a vast array of actions, many of them opposite to those attributed to the main effector peptide of the RAS, Ang II. The discovery of the Ang-converting enzyme (ACE) homolog ACE2 brought to light an important metabolic pathway responsible for Ang-(1-7) synthesis. This enzyme can form Ang-(1-7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1-9) with subsequent Ang-(1-7) formation by ACE. In addition, it is now well established that the G protein-coupled receptor Mas is a functional binding site for Ang-(1-7). Thus, the axis formed by ACE2/Ang-(1-7)/Mas appears to represent an endogenous counterregulatory pathway within the RAS, the actions of which are in opposition to the vasoconstrictor/ proliferative arm of the RAS consisting of ACE, Ang II, and AT 1 receptor. In this brief review, we will discuss recent findings related to the biological role of the ACE2/Ang-(1-7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism. In addition, we will highlight the potential interactions of Ang-(1-7) and Mas with AT 1 and AT 2 receptors.

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ACE2–angiotensin-(1–7)–Mas axis in renal ischaemia/reperfusion injury in rats

Cited by 98 publications

References 41 publications

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

Association of Elevated Urinary Concentration of Renin-Angiotensin System Components and Severe AKI

Angiotensin-converting enzyme 2, angiotensin-(1–7) and Mas: new players of the renin–angiotensin system

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