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      Aliskiren Reduces the Adrenal Zona Glomerulosa Apoptosis and Autophagy in Wistar Rats with 2K1C Hypertension

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          Abstract

          Hypertension is a disease classified as primary or secondary, manifested not only by elevation of blood pressure but also involved in structural and functional changes of target organs. Renal artery stenosis is a leading factor of secondary hypertension, and its progress is associated with overactivation of the renin-angiotensin-aldosterone system (RAAS). Aliskiren is a renin inhibiting drug that suppresses RAAS and culminates in decreased renin release, plasma angiotensin II concentration, and inhibition of aldosterone secretion. In this sense, the aim of the present study was to analyze the structural and ultrastructural morphophysiology of the adrenal glomerular zone, after treatment with aliskiren in Wistar rats with 2K1C hypertension. Parameters as structure and ultrastructure of the adrenal glomerular zone, cellular apoptosis, nuclear cell proliferation, and AT1 receptor expression were analyzed by immunostaining and electron microscopy. Our results showed that the hypertensive animals treated with aliskiren presented a reestablishment of AT1 receptor expression and decrease in apoptosis and autophagy. In addition, treatment with aliskiren improves the cell aspects in the adrenal glomerular zone, evidenced by ultrastructural analysis through preserved nuclei and well-developed mitochondria. Therefore, our evidence suggests that aliskiren has a beneficial effect on the adrenal glomerular zone remodeling in animals with renovascular hypertension.

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          Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies.

          Sarah Lewington, Robert Clarke, Nawab Qizilbash … (2003)
          The age-specific relevance of blood pressure to cause-specific mortality is best assessed by collaborative meta-analysis of individual participant data from the separate prospective studies. Information was obtained on each of one million adults with no previous vascular disease recorded at baseline in 61 prospective observational studies of blood pressure and mortality. During 12.7 million person-years at risk, there were about 56000 vascular deaths (12000 stroke, 34000 ischaemic heart disease [IHD], 10000 other vascular) and 66000 other deaths at ages 40-89 years. Meta-analyses, involving "time-dependent" correction for regression dilution, related mortality during each decade of age at death to the estimated usual blood pressure at the start of that decade. Within each decade of age at death, the proportional difference in the risk of vascular death associated with a given absolute difference in usual blood pressure is about the same down to at least 115 mm Hg usual systolic blood pressure (SBP) and 75 mm Hg usual diastolic blood pressure (DBP), below which there is little evidence. At ages 40-69 years, each difference of 20 mm Hg usual SBP (or, approximately equivalently, 10 mm Hg usual DBP) is associated with more than a twofold difference in the stroke death rate, and with twofold differences in the death rates from IHD and from other vascular causes. All of these proportional differences in vascular mortality are about half as extreme at ages 80-89 years as at ages 40-49 years, but the annual absolute differences in risk are greater in old age. The age-specific associations are similar for men and women, and for cerebral haemorrhage and cerebral ischaemia. For predicting vascular mortality from a single blood pressure measurement, the average of SBP and DBP is slightly more informative than either alone, and pulse pressure is much less informative. Throughout middle and old age, usual blood pressure is strongly and directly related to vascular (and overall) mortality, without any evidence of a threshold down to at least 115/75 mm Hg.
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            Telomere dysfunction induces metabolic and mitochondrial compromise.

            Ergun Sahin, Simona Colla, Marc Liesa … (2011)
            Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1α and PGC-1β, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1α expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1α and PGC-1β promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.
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              Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network.

              Richard C Scarpulla (2011)
              The PGC-1 family of regulated coactivators, consisting of PGC-1α, PGC-1β and PRC, plays a central role in a regulatory network governing the transcriptional control of mitochondrial biogenesis and respiratory function. These coactivators target multiple transcription factors including NRF-1, NRF-2 and the orphan nuclear hormone receptor, ERRα, among others. In addition, they themselves are the targets of coactivator and co-repressor complexes that regulate gene expression through chromatin remodeling. The expression of PGC-1 family members is modulated by extracellular signals controlling metabolism, differentiation or cell growth and in some cases their activities are known to be regulated by post-translational modification by the energy sensors, AMPK and SIRT1. Recent gene knockout and silencing studies of many members of the PGC-1 network have revealed phenotypes of wide ranging severity suggestive of complex compensatory interactions or broadly integrative functions that are not exclusive to mitochondrial biogenesis. The results point to a central role for the PGC-1 family in integrating mitochondrial biogenesis and energy production with many diverse cellular functions. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection. Copyright © 2010 Elsevier B.V. All rights reserved.
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                Author and article information

                Contributors
                Veronica S. de Matos:
                ORCID: https://orcid.org/0000-0001-9954-1007
                Aline Bonfim Vieira:
                ORCID: https://orcid.org/0000-0002-2479-6774
                Jemima F. R. da Silva:
                ORCID: https://orcid.org/0000-0001-7867-3131
                Jorge J. de Carvalho:
                ORCID: https://orcid.org/0000-0002-9426-6381
                Journal
                Journal ID (nlm-ta): Int J Hypertens
                Journal ID (iso-abbrev): Int J Hypertens
                Journal ID (publisher-id): ijhy
                Title: International Journal of Hypertension
                Publisher: Hindawi
                ISSN (Print): 2090-0384
                ISSN (Electronic): 2090-0392
                Publication date Collection: 2020
                Publication date (Electronic): 21 October 2020
                Volume: 2020
                Electronic Location Identifier: 7684849
                Affiliations
                1Laboratory of Ultrastructure and Tecidual Biology, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil
                2Translational Endocrinology Laboratory, Institute of Biophysics Carlos Chagas Filho, Health Sciences Center, UFRJ, Rio de Janeiro, Brazil
                3Institute of Biology, UFF, Rio de Janeiro, RJ, Brazil
                4National Commission of Nuclear Energy, CNEN, Rio de Janeiro, Brazil
                5Ross University School of Veterinary Medicine, Biomedical Department, Basseterre, Saint Kitts and Nevis
                Author notes

                Academic Editor: Tomohiro Katsuya

                Author information
                https://orcid.org/0000-0001-9954-1007
                https://orcid.org/0000-0002-2479-6774
                https://orcid.org/0000-0001-7867-3131
                https://orcid.org/0000-0002-9426-6381
                Article
                DOI: 10.1155/2020/7684849
                PMC ID: 7596424
                SO-VID: 52ef29f5-db47-4e5a-952c-aa3887819a66
                Copyright © Copyright © 2020 Veronica S. de Matos et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 June 2020
                Date revision received : 21 August 2020
                Date accepted : 4 September 2020
                Funding
                Funded by: Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro
                Funded by: Conselho Nacional de Desenvolvimento Científico e Tecnológico
                Funded by: Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
                Funded by: Universidade do Estado do Rio de Janeiro
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Cardiovascular Medicine
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine

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