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      Exercise Training Can Prevent Cardiac Hypertrophy Induced by Sympathetic Hyperactivity with Modulation of Kallikrein-Kinin Pathway and Angiogenesis

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          Abstract

          Sympathetic hyperactivity induces adverse effects in myocardial. Recent studies have shown that exercise training induces cardioprotection against sympathetic overload; however, relevant mechanisms of this issue remain unclear. We analyzed whether exercise can prevent pathological hypertrophy induced by sympathetic hyperactivity with modulation of the kallikrein-kinin and angiogenesis pathways. Male Wistar rats were assigned to non-trained group that received vehicle; non-trained isoproterenol treated group (Iso, 0.3 mg kg −1 day −1); and trained group (Iso+Exe) which was subjected to sympathetic hyperactivity with isoproterenol. The Iso rats showed hypertrophy and myocardial dysfunction with reduced force development and relaxation of muscle. The isoproterenol induced severe fibrosis, apoptosis and reduced myocardial capillary. Interestingly, exercise blunted hypertrophy, myocardial dysfunction, fibrosis, apoptosis and capillary decreases. The sympathetic hyperactivity was associated with high abundance of ANF mRNA and β-MHC mRNA, which was significantly attenuated by exercise. The tissue kallikrein was augmented in the Iso+Exe group, and kinin B 1 receptor mRNA was increased in the Iso group. Moreover, exercise induced an increase of kinin B 2 receptor mRNA in myocardial. The myocardial content of eNOS, VEGF, VEGF receptor 2, pAkt and Bcl-2 were increased in the Iso+Exe group. Likewise, increased expression of pro-apoptotic Bad in the Iso rats was prevented by prior exercise. Our results represent the first demonstration that exercise can modulate kallikrein-kinin and angiogenesis pathways in the myocardial on sympathetic hyperactivity. These findings suggest that kallikrein-kinin and angiogenesis may have a key role in protecting the heart.

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          Progression from compensated hypertrophy to failure in the pressure-overloaded human heart: structural deterioration and compensatory mechanisms.

          The progression of compensated hypertrophy to heart failure (HF) is still debated. We investigated patients with isolated valvular aortic stenosis and differing degrees of left ventricular (LV) systolic dysfunction to test the hypothesis that structural remodeling, as well as cell death, contributes to the transition to HF. Structural alterations were studied in LV myectomies from 3 groups of patients (group 1: ejection fraction [EF] >50%, n=12; group 2: EF 30% to 50%, n=12; group 3: EF <30%, n=10) undergoing aortic valve replacement. Control patients were patients with mitral valve stenosis but normal LV (n=6). Myocyte hypertrophy was accompanied by increased nuclear DNA and Sc-35 (splicing factor) content. ACE and TGF-beta1 were upregulated correlating with fibrosis, which increased 2.3-, 2.2-, and 3.2-fold over control in the 3 groups. Myocyte degeneration increased 10, 22, and 32 times over control. A significant correlation exists between EF and myocyte degeneration or fibrosis. Ubiquitin-related autophagic cell death was 0.5 per thousand in control and group 1, 1.05 in group 2, and 6.05 per thousand in group 3. Death by oncosis was 0 per thousand in control, 3 per thousand in group 1, and increased to 5 per thousand (groups 2 and 3). Apoptosis was not detectable in control and group 3, but it was present at 0.02 per thousand in group 1 and 0.01 per thousand in group 2. Cardiomyocyte mitosis was never observed. These structure-function correlations confirm the hypothesis that transition to HF occurs by fibrosis and myocyte degeneration partially compensated by hypertrophy involving DNA synthesis and transcription. Cell loss, mainly by autophagy and oncosis, contributes significantly to the progression of LV systolic dysfunction.
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            Control of cardiac muscle cell function by an endogenous nitric oxide signaling system.

            Nitric oxide (NO) synthesized from L-arginine is a ubiquitous intracellular chemical messenger and is involved in signal transduction in diverse mammalian cells, including vascular endothelium and neuronal tissues. The role of the NO-signaling pathway in the direct modulation of cardiac function is less well characterized. In this report, the effects of inhibitors of NO synthase (NOS) were examined in isolated neonatal and adult rat ventricular myocytes exposed to either muscarinic or adrenergic agonists. Carbachol (10 microM) caused a 91% inhibition of the spontaneous beating rate of cultured neonatal rat cardiac myocytes. N omega-monomethyl-L-arginine, an L-arginine analog that inhibits NOS, and methylene blue, an inhibitor of NO, blocked the negative chronotropic effect of carbachol but had no effect on the basal beating rate of these cells. The inhibition by N omega-monomethyl-L-arginine of the negative chronotropic effect of carbachol was reversed by adding excess L-arginine. The negative chronotropic effect of carbachol was also mimicked by analogs of cGMP, a second messenger implicated in mediating the action of NO in other cell types. Production of NO could be detected directly in carbachol-stimulated neonatal myocytes by using a reporter cell bioassay. The regulation of adrenergic responsiveness by the NO signaling system was also documented in studies of adult cardiac myocyte contractility. The NOS inhibitor N omega-nitro-L-arginine significantly increased the inotropic effect of the beta-adrenergic agonist isoproterenol on electrically stimulated adult rat ventricular myocytes, whereas this inhibitor had no effect on basal contractility. Inhibition of NO production by N omega-monomethyl-L-arginine in these cells, as measured by reporter cell bioassay, was also reversible with excess L-arginine. Thus, the physiologic response of isolated neonatal and adult ventricular myocytes to both muscarinic cholinergic and beta-adrenergic stimulation is mediated, at least in part, by products of an endogenous NOS.
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              Physical activity and pregnancy: past and present evidence and future recommendations.

              In this review, we provide researchers and practitioners with an overview of the physical activity and pregnancy literature to promote prenatal physical activity, improve measurement, further elucidate the role of activity in reducing maternal health complications, and inform future research. We examined past and present physical activity and pregnancy studies and highlight key papers with a focus on maternal health outcomes to best inform physical activity promotion efforts. We discuss: (a) historical overview of prenatal physical activity relative to the physical activity guidelines, how they have changed over time, and how evidence of the effect of prenatal activity on maternal/fetal health outcomes has affected clinical recommendations; (b) existing tools and challenges associated with measuring prenatal physical activity; (c) empirical evidence on multilevel determinants of prenatal activity to guide future intervention work; (d) empirical evidence of prenatal activity on adverse maternal outcomes (gestational diabetes mellitus, preeclampsia, excessive gestational weight gain) from observational and intervention studies; and (e) summary/recommendations for future research and practice. The physical activity and pregnancy literature has evolved over the past 50 years, and there is sufficient empirical evidence to support the promotion of moderate-to-vigorous prenatal physical activity for maternal health benefits. Future studies and interventions should be carefully designed, theoretically driven, and include validated and reliable activity measures. Researchers and practitioners should also consider the multifaceted determinants and outcomes of prenatal physical activity and intervene to promote physical activity before, during, and after pregnancy.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2014
                10 March 2014
                : 9
                : 3
                : e91017
                Affiliations
                [1 ]Universidade Nove de Julho (Uninove), Programa de Pós-graduação em Ciências da Reabilitação, Rua Vergueiro, São Paulo, SP, Brazil
                [2 ]Universidade Federal de São Paulo (Unifesp), Rua Napoleão de Barros, São Paulo, SP, Brazil
                [3 ]Universidade de São Paulo, Incor. Av. Dr. Enéas de Carvalho Aguiar, São Paulo, SP, Brazil
                [4 ]Universidade Nove de Julho (Uninove), Programa de Pós-graduação em Medicina, Rua Vergueiro, São Paulo, SP, Brazil
                UAE University, Faculty of Medicine & Health Sciences, United Arab Emirates
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: JAS AJS. Performed the experiments: JAS ETS MTM ELA DSB. Analyzed the data: JAS AJS PJFT. Contributed reagents/materials/analysis tools: JEK PJFT. Wrote the paper: JAS AJS.

                Article
                PONE-D-13-42409
                10.1371/journal.pone.0091017
                3948752
                24614810
                4992727d-c466-462f-9a85-3ca6fdeae6e5
                Copyright @ 2014

                et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 16 October 2013
                : 7 February 2014
                Page count
                Pages: 9
                Funding
                This work was supported by grant number 2009/54225-8, São Paulo Research Foundation (FAPESP) and National Council for Scientific and Technological (grant numbers 477458/2009-2; 479395/2012-8). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Biology
                Anatomy and Physiology
                Cardiovascular System
                Developmental Biology
                Morphogenesis
                Cell Migration
                Molecular Cell Biology
                Signal Transduction
                Signaling Pathways
                Medicine
                Cardiovascular
                Heart Failure
                Critical Care and Emergency Medicine
                Acute Cardiovascular Problems
                Oncology
                Cancer Treatment
                Antiangiogenesis Therapy
                Primary Care
                Sports and Exercise Medicine

                Uncategorized
                Uncategorized

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