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      Angiotensin-(1–7) and the renin–angiotensin system

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          Abstract

          In this review we will focus on the recent findings related to angiotensin-(1-7) as an angiotensin II counter-regulatory peptide within the renin-angiotensin system. The identification of the angiotensin-converting enzyme homologue ACE2 as an angiotensin peptide processing enzyme and of Mas as a receptor for angiotensin-(1-7) has contributed to establishing this heptapeptide as a biologically active member of the renin-angiotensin system cascade. The previously unsuspected complexity of the renin-angiotensin system, unmasked by novel findings, has revealed new possibilities for exploring its physiological and pathophysiological roles. In addition, the ACE2-angiotensin-(1-7)-Mas axis may be seriously considered as a putative target for the development of new cardiovascular drugs.

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          Newly recognized components of the renin-angiotensin system: potential roles in cardiovascular and renal regulation.

          Megan R Carey, Helmy M. Siragy (2003)
          The renin-angiotensin system (RAS) is a coordinated hormonal cascade in the control of cardiovascular, renal, and adrenal function that governs body fluid and electrolyte balance, as well as arterial pressure. The classical RAS consists of a circulating endocrine system in which the principal effector hormone is angiotensin (ANG) II. ANG is produced by the action of renin on angiotensinogen to form ANG I and its subsequent conversion to the biologically active octapeptide by ANG-converting enzyme. ANG II actions are mediated via the ANG type 1 receptor. Here, we discuss recent advances in our understanding of the components and actions of the RAS, including local tissue RASs, a renin receptor, ANG-converting enzyme-2, ANG (1-7), the function of the ANG type 2 receptor, and ANG receptor heterodimerization. The role of the RAS in the regulation of cardiovascular and renal function is reviewed and discussed in light of these newly recognized components.
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            Angiotensin-(1-7): cardioprotective effect in myocardial ischemia/reperfusion.

            Luisa Ferreira, Fabio A. Almeida, Rinaldo dos Santos … (2001)
            In this study we evaluate the effects of angiotensin-(1-7) on reperfusion arrhythmias in isolated rat hearts. Rat hearts were perfused according to Langendorff technique and maintained in heated (37+/-1 degrees C) and continuously gassed (95% O(2)/5% CO(2)) Krebs-Ringer solution at constant pressure (65 mm Hg). The electrical activity was recorded with an ECG (bipolar). Local ischemia was induced by coronary ligation for 15 minutes. After ischemia, hearts were reperfused for 30 minutes. Cardiac arrhythmias were defined as the presence of ventricular tachycardia and/or ventricular fibrillation after the ligation of the coronary artery was released. Angiotensin II (0.20 nmol/L, n=10) produced a significant enhancement of reperfusion arrhythmias. On the other hand, Ang-(1-7) presented in the perfusion solution (0.22 nmol/L, n=11) reduced incidence and duration of arrhythmias. The antiarrhythmogenic effects of Ang-(1-7) was blocked by the selective Ang-(1-7) antagonist A-779 (2 nmol/L, n=9) and by indomethacin pretreatment (5 mg/kg IP, n=8) but not by the bradykinin B(2) antagonist HOE 140 (100 nmol/L, n=10) or by L-NAME pretreatment (30 mg/kg IP, n=8). These results suggest that the antiarrhythmogenic effect of low concentrations of Ang-(1-7) is mediated by a specific receptor and that release of endogenous prostaglandins.by Ang-(1-7) contributes to the alleviation of reversible and/or irreversible ischemia-reperfusion injury.
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              Impairment of in vitro and in vivo heart function in angiotensin-(1-7) receptor MAS knockout mice.

              Jaqueline Cruz, Vanessa de Jesus R de Paula, Osvaldo P. Almeida … (2006)
              In this study we investigated the effects of the genetic deletion of the angiotensin (Ang)-(1-7) receptor Mas on heart function. Localization of Mas in the mouse heart was evaluated by binding of rhodamine-labeled Ang-(1-7). Cardiac function was examined using isolated heart preparations. Echocardiography was used to confirm the results obtained with isolated heart studies. To elucidate the possible mechanisms involved in the cardiac phenotype observed in Mas(-/-) mice, whole-cell calcium currents in cardiomyocytes and the expression of collagen types I, III, and VI and fibronectin were analyzed. Ang-(1-7) binding showed that Mas is localized in cardiomyocytes of the mouse heart. Isolated heart techniques revealed that Mas-deficient mice present a lower systolic tension (average: 1.4+/-0.09 versus 2.1+/-0.03 g in Mas(+/+) mice), +/-dT/dt, and heart rate. A significantly higher coronary vessel resistance was also observed in Mas-deficient mice. Echocardiography revealed that hearts of Mas-deficient mice showed a significantly decreased fractional shortening, posterior wall thickness in systole and left ventricle end-diastolic dimension, and a higher left ventricle end-systolic dimension. A markedly lower global ventricular function, as defined by a higher myocardial performance index, was observed. A higher delayed time to the peak of calcium current was also observed. The changes in cardiac function could be partially explained by a marked change in collagen expression to a profibrotic profile in Mas-deficient mice. These results indicate that Ang-(1-7)-Mas axis plays a key role in the maintenance of the structure and function of the heart.
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                Author and article information

                Journal
                Title: Current Opinion in Nephrology and Hypertension
                Abbreviated Title: Current Opinion in Nephrology and Hypertension
                Publisher: Ovid Technologies (Wolters Kluwer Health)
                ISSN (Print): 1062-4821
                Publication date Created: 2007
                Publication date (Print): March 2007
                Volume: 16
                Issue: 2
                Pages: 122-128
                Article
                DOI: 10.1097/MNH.0b013e328031f362
                PubMed ID: 17293687
                SO-VID: 97332adf-d1d2-4683-b7b0-7469f95b1d6d
                Copyright © © 2007
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