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      • Record: found
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      Angiotensin (1-7) and apelin co-therapy: New strategy for heart failure treatment in rats

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          Abstract

          Objective:

          Isoproterenol (ISO)–induced heart failure is a standardized model for the study of beneficial effects of various drugs. Both apelin and angiotensin 1–7 have a cardiac protective effect. We assumed that co–therapy with apelin and angiotensin 1–7 [Ang (1–7)] may have synergistic cardioprotective effects against isoproterenol-induced heart failure.

          Methods:

          The rats were randomly assigned to one of eight groups, 7 animals in each, as follows: (1) Control I (saline; IP injection), (2) Control II (saline; via mini-osmotic pump), (3) ISO (5 mg/kg; IP), (4) Apelin (20 μg/kg; IP), (5) Ang (1–7) (30 μg/kg/day; via mini-osmotic pump), (6) Apelin+ISO, (7) Ang (1–7)+ISO, and (8) Apelin+Ang (1–7)+ISO. Rat myocardial injury was induced by intraperitoneal injection of 5 mg/kg of ISO for 10 days. Apelin and Ang (1–7) were administered 30 minutes before the ISO injection.

          Results:

          A decrease in the systolic blood pressure [SBP (p<0.001)], diastolic blood pressure [DBP (p=0.024)], left ventricular systolic pressure [LVSP (p<0.001)], left ventricular contractility [dP/dt max. (p<0.001)], relaxation [dP/dt min. (p<0.001)], and an increase in left ventricular end-diastolic pressure [LVEDP, (p<0.001)] were observed in ISO-treated rats. Plasma LDH and myocardial and plasma MDA were higher in the ISO heart than in controls (p<0.001). Histopathological examination of the cardiac tissue showed myocardial fibrosis and leukocyte infiltration in ISO-treated rats as compared to control. Co-therapy with apelin and Ang (1–7) was more effective than either agent used alone in restoring these parameters to that of control rats.

          Conclusion:

          The results of this study showed that the combination of apelin and Ang (1–7) had a more cardioprotective effect than either used alone against ISO-induced heart failure, and co–therapy may be a useful treatment option for myocardial injuries and heart failure.

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          Most cited references26

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          The novel peptide apelin lowers blood pressure via a nitric oxide-dependent mechanism.

          Kazuhiko Tatemoto, Kiyoshige Takayama, Min-Xu Zou … (2001)
          Apelin is an endogenous ligand of the human orphan receptor APJ. We detected apelin-like immunoreactivity in the adipocytes, gastric mucosa, and Kupffer cells in the liver. We also detected apelin-like immunoreactivity localized within the endothelia of small arteries in various organs. Further, it was found that mean arterial pressure after the administration of apelin-12, apelin-13, and apelin-36 at a dose of 10 nmol/kg in anaesthetized rats was reduced by 26+/-5, 11+/-4, and 5+/-4 mm Hg, respectively. In the presence of a nitric oxide (NO) synthase inhibitor, the effect of apelin-12 on blood pressure was abolished. Furthermore, the administration of apelin-12 (10 nmol/kg) in rats produced a transitory elevation of the plasma nitrite/nitrate concentration from a basal level of 21.4+/-1.6 to 27.0+/-1.5 microM. Thus, apelin may lower blood pressure via a nitric oxide-dependent mechanism.
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            Catecholamine cardiotoxicity.

            G Rona (1985)
            The morphologic-functional correlative studies that we have carried out in the past 25 years with the various catecholamines have served as an example for analyzing myocardial reaction patterns and the reactions of the cardiac muscle cells to insult. These studies disclosed the unique nature of isoproterenol in producing 'infarct-like' myocardial necrosis. It appears that the pathogenesis of the catecholamine-induced myocardial necrosis is multifactorial. Our early studies suggested the role of relative hypoxia. Later studies by using extracellular fine structural protein tracers demonstrated the importance of microcirculatory effects as well as, in the norepinephrine model, that of early sarcolemmal membrane permeability alteration. The Ca2+ overload theory is supported not only by the experimental observations but also by its successful application in clinical cardiology. A new contribution is the recognition of catecholamine oxidation products in producing myocardial injury. Experimental data indicate that catecholamines play an important role in reperfusion and ischemic myocardial injuries. The sequence of events demonstrated by our studies with catecholamines might represent a common pathway in the evolution of myocardial changes in humans who develop myocardial lesions without narrowing or obstruction of coronary arteries. Investigation in the field of molecular and cellular cardiology has led to a better understanding of current clinical problems and helped to devise procedures for the prevention and management of human myocardial disorders. The isoproterenol-induced myocardial necrosis served as model to Professor A. Fleckenstein to formulate the Ca2+ overload theory of myocardial injury and develop a series of now widely used Ca2+ antagonistic drugs for the management and the prevention of human myocardial diseases.
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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.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Anatol J Cardiol
                Journal ID (iso-abbrev): Anatol J Cardiol
                Title: Anatolian Journal of Cardiology
                Publisher: Kare Publishing (Turkey )
                ISSN (Print): 2149-2263
                ISSN (Electronic): 2149-2271
                Publication date (Print): 2020
                Publication date (Electronic): 18 February 2020
                Volume: 23
                Issue: 4
                Pages: 209-217
                Affiliations
                [* ]Department of Physiology, and Fasa University of Medical Sciences; Fasa- Iran
                [** ]Department Pathology, Fasa University of Medical Sciences; Fasa- Iran
                [*** ]Department Internal Medicine, Fasa University of Medical Sciences; Fasa- Iran
                Author notes
                Address for correspondence: Kazem Javanmardi, PhD, Department of Physiology, Fasa University of Medical Sciences, Ebn-E-Sina SQ, Fasa- Iran Phone: 00987153350994 Fax: 00987153357091 E-mail: kjavanmardi@fums.ac.ir - kjavanmardi@ 123456gmail.com
                Article
                Publisher ID: AJC-23-209
                DOI: 10.14744/AnatolJCardiol.2019.40072
                PMC ID: 7163218
                PubMed ID: 32235135
                SO-VID: 3f0db601-7b64-4eee-add9-eab383a87dba
                Copyright © Copyright: © 2020 Turkish Society of Cardiology
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

                History
                Date accepted : 03 December 2019
                Categories
                Subject: Original Investigation

                Keywords: apelin,ang (1–7),heart failure,isoproterenol,rat
                Data availability:
                Keywords: apelin, ang (1–7), heart failure, isoproterenol, rat

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