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      Regulation of angiotensin-(1–7) and angiotensin II type 1 receptor by telmisartan and losartan in adriamycin-induced rat heart failure

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          Abstract

          Aim:

          To investigate the possible effects of telmisartan and losartan on cardiac function in adriamycin (ADR)-induced heart failure in rats, and to explore the changes in plasma level of angiotensin-(1–7)[Ang-(1–7)] and myocardial expression of angiotensin II type 1/2 receptors (AT1R / AT2R) and Mas receptor caused by the two drugs.

          Methods:

          Male Sprague-Dawley rats were randomly divided into 4 groups: the control group, ADR-treated heart failure group (ADR-HF), telmisartan plus ADR-treated group (Tel+ADR) and losartan plus ADR-treated group (Los+ADR). ADR was administrated (2.5 mg/kg, ip, 6 times in 2 weeks). The rats in the Tel+ADR and Los+ADR groups were treated orally with telmisartan (10 mg/kg daily po) and losartan (30 mg/kg daily), respectively, for 6 weeks. The plasma level of Ang-(1–7) was determined using ELISA. The mRNA and protein expression of myocardial Mas receptor, AT 1R and AT 2R were measured using RT-PCR and Western blotting, respectively.

          Results:

          ADR significantly reduced the plasma level of Ang-(1–7) and the expression of myocardial Mas receptor and myocardial AT 2R, while significantly increased the expression of myocardial AT1R. Treatment with telmisartan and losartan effectively increased the plasma level of Ang-(1–7) and suppressed myocardial AT1R expression, but did not influence the expression of Mas receptor and AT 2R.

          Conclusion:

          The protective effects of telmisartan and losartan in ADR-induced heart failure may be partially due to regulation of circulating Ang-(1–7) and myocardial AT1R expression.

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          Most cited references22

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          Renin-angiotensin system and cardiovascular risk.

          Roland E Schmieder, Bernhard Schmidt, Markus P. Schlaich … (2007)
          The renin-angiotensin system is a major regulatory system of cardiovascular and renal function. Basic research has revealed exciting new aspects, which could lead to novel or modified therapeutic approaches. Renin-angiotensin system blockade exerts potent antiatherosclerotic effects, which are mediated by their antihypertensive, anti-inflammatory, antiproliferative, and oxidative stress lowering properties. Inhibitors of the system-ie, angiotensin converting enzyme inhibitors and angiotensin receptor blockers, are now first-line treatments for hypertensive target organ damage and progressive renal disease. Their effects are greater than expected by their ability to lower blood pressure alone. Angiotensin receptor blockers reduce the frequency of atrial fibrillation and stroke. Renin-angiotensin system blockade delays or avoids the onset of type 2 diabetes and prevents cardiovascular and renal events in diabetic patients. Thus, blockade of this system will remain a cornerstone of our strategies to reduce cardiovascular risk.
          Article 0 comments Cited 143 times – based on 0 reviews     Review now
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            Endothelial progenitor cell transplantation improves long-term stroke outcome in mice.

            Yuan Yang, Jianrong Liu, Tim Frenzel … (2010)
            Endothelial progenitor cells (EPCs) play an important role in tissue repairing and regeneration in ischemic organs, including the brain. However, the cause of EPC migration and the function of EPCs after ischemia are unclear. In this study, we demonstrated the effects of EPCs on ischemic brain injury in a mouse model of transient middle cerebral artery occlusion (tMCAO). Circulating human EPCs were characterized with immunofluorescent staining and flow cytometry. EPCs (1 x 10(6)) were injected into nude mice after 1 hour of tMCAO. Histological analysis and behavioral tests were performed from day 0 to 28 days after tMCAO. EPCs were detected in ischemic brain regions 24 hours after tMCAO. EPC transplantation significantly reduced ischemic infarct volume at 3 days after tMCAO compared with control animals (p < 0.05). CXCR4 was expressed in the majority of EPCs, and stromal-derived factor-1 (SDF-1) induced EPC migration, which was blocked by pretreated EPCs with AMD3100 in vitro. SDF-1 was upregulated in ischemic brain. Compared with control animals, injecting AMD3100-pretreated EPCs resulted in a larger infarct volume 3 days after tMCAO, suggesting that SDF-1-mediated signaling was involved in EPC-mediated neuroprotection. In addition, EPC transplantation reduced mouse cortex atrophy 4 weeks after tMCAO and improved neurobehavioral outcomes (p < 0.05). EPC injection potently increased angiogenesis in the peri-infarction area (p < 0.05). We conclude that systemic delivery of EPCs protects the brain against ischemic injury, promotes neurovascular repair, and improves long-term neurobehavioral outcomes. Our data suggest that SDF-1-mediated signaling plays a critical role in EPC-mediated neuroprotection.
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              Prevention of angiotensin II-induced cardiac remodeling by angiotensin-(1-7).

              M Lingis, T Bolton, Michael J Katovich … (2007)
              Cardiac remodeling, which typically results from chronic hypertension or following an acute myocardial infarction, is a major risk factor for the development of heart failure and, ultimately, death. The renin-angiotensin system (RAS) has previously been established to play an important role in the progression of cardiac remodeling, and inhibition of a hyperactive RAS provides protection from cardiac remodeling and subsequent heart failure. Our previous studies have demonstrated that overexpression of angiotensin-converting enzyme 2 (ACE2) prevents cardiac remodeling and hypertrophy during chronic infusion of angiotensin II (ANG II). This, coupled with the knowledge that ACE2 is a key enzyme in the formation of ANG-(1-7), led us to hypothesize that chronic infusion of ANG-(1-7) would prevent cardiac remodeling induced by chronic infusion of ANG II. Infusion of ANG II into adult Sprague-Dawley rats resulted in significantly increased blood pressure, myocyte hypertrophy, and midmyocardial interstitial fibrosis. Coinfusion of ANG-(1-7) resulted in significant attenuations of myocyte hypertrophy and interstitial fibrosis, without significant effects on blood pressure. In a subgroup of animals also administered [d-Ala(7)]-ANG-(1-7) (A779), an antagonist to the reported receptor for ANG-(1-7), there was a tendency to attenuate the antiremodeling effects of ANG-(1-7). Chronic infusion of ANG II, with or without coinfusion of ANG-(1-7), had no effect on ANG II type 1 or type 2 receptor binding in cardiac tissue. Together, these findings indicate an antiremodeling role for ANG-(1-7) in cardiac tissue, which is not mediated through modulation of blood pressure or altered cardiac angiotensin receptor populations and may be at least partially mediated through an ANG-(1-7) receptor.
              Article 0 comments Cited 85 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Acta Pharmacol Sin
                Journal ID (iso-abbrev): Acta Pharmacol. Sin
                Title: Acta Pharmacologica Sinica
                Publisher: Nature Publishing Group
                ISSN (Print): 1671-4083
                ISSN (Electronic): 1745-7254
                Publication date (Print): November 2011
                Publication date (Electronic): 03 October 2011
                Volume: 32
                Issue: 11
                Pages: 1345-1350
                Affiliations
                [1 ]Department of Cardiology, First Affiliated Hospital, Nanjing Medical University , Nanjing 210029, China
                Author notes
                [#]

                The first two authors contributed equally to this work.

                Article
                Publisher Item ID: aps201196
                DOI: 10.1038/aps.2011.96
                PMC ID: 4002738
                PubMed ID: 21963897
                SO-VID: 1c5a0c59-6337-4fd6-aaaa-a286240a6d88
                Copyright © Copyright © 2011 CPS and SIMM
                History
                Date received : 31 December 2010
                Date accepted : 21 June 2011
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: angiotensin-(1–7),mas,angiotensin i receptor,angiotensin ii receptor,adriamycin,heart failure,telmisartan,losartan
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: angiotensin-(1–7), mas, angiotensin i receptor, angiotensin ii receptor, adriamycin, heart failure, telmisartan, losartan

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