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The Protective Arm of the Renin Angiotensin System: Functional Aspects and Therapeutic Implications is the first comprehensive publication to signal the protective role of a distinct part of the renin–angiotensin system (RAS), providing readers with early insight into a complex system which will become of major medical importance in the near future. Focusing on recent research, The Protective Arm of the Renin Angiotensin System presents a host of new experimental studies on specific components of the RAS, namely angiotensin AT2 receptors (AT2R), the angiotensin (1–7) peptide with its receptor Mas, and the enzyme ACE 2, which exert significant beneficial, health-promoting actions by counterbalancing the well-known harmful arm of the RAS with its classical angiotensin AT1 receptor. This innovative concept of the protective arm of the RAS, examined in this reference, represents an indispensable background and will be a strong support for biomedical students, researchers, cardiologists, surgeons, nephrologists, diabetologists, and endocrinologists, as well as any other physician or researcher concerned with RAS physiology, pathophysiology and clinical implications. - Provides a complete understanding of the protective side of the Renin Angiotensin System (RAS) involving angiotensin AT2 receptor, ACE2, and Ang(1-7)/Mas receptor - Combines the knowledge of editors who pioneered research on the protective renin angiotensin system including; Dr. Thomas Unger, one of the founders of AT2 receptor research; Dr. Ulrike M. Steckelings, who contributed significantly to first preclinical studies with a novel specific AT2-agonist, and Dr. Robson Santos who pioneered research on angiotensin-(1-7) and its receptor Mas. - Shows that the protective RAS axes are able to ameliorate the course of several cardiovascular, renal, metabolic and neurological diseases - Provides the basis for the understanding of a novel therapeutic approach to stimulate components of the protective arm of the RAS.
Angiotensin-converting enzyme 2 (ACE2) is the primary enzyme of the vasoprotective axis of the renin-angiotensin system (RAS). We tested the hypothesis that the protective arm of the RAS axis can i) act to maintain homeostasis in the diabetic bone marrow stem cell compartment, ii) regulate the reparative function of the hematopoietic stem/progenitor cells (HSPCs) and iii) modulate the gut microbiota composition. All processes could influence the development of diabetic retinopathy. Diabetic ACE2 knockout (KO)/C57BL/6-Ins2WT/C96Y (Akita) mice were examined at 3 and 9 months after the onset of diabetes and compared to age-matched controls. Both ACE2KO-Akita and Akita cohorts showed reduced retinal thickness by optical coherence tomography at 9 months of diabetes. The absence of ACE2 in 9-month diabetic mice led to an accelerated increase in acellular capillaries, a hallmark feature of diabetic retinopathy. The absence of ACE2 also caused a reduction of both long-term and short-term repopulating HSPCs in the diabetic bone marrow at 9 months of diabetes. Reparative function studies showed that ACE2KO exacerbated diabetes-induced impairment of lineage-c-kit+ HSPC migration and proliferation as early as 3-month of diabetes. HSPCs from both early and late stage diabetic mice, pretreated with Ang-(1-7) or alamandine (two downstream peptides of ACE2) showed restored migration and proliferation. The gut microbiota has been implicated in the pathogenesis of diabetes. Analysis of the gut microbiome also revealed a distinct bacterial profile in ACE2KO-Akita group, with a great diversity of bacterial types that were previously reported to contribute to diabetic pathogenesis, including Tenericutes at the phylum level and Mollicutes at the class level, and with an activation of peptidoglycan biosynthesis pathways. Flow cytometry analysis showed that loss of ACE2 led to less infiltration of circulating angiogenic cells in the gut which may lead to an increased endothelial cell permeability in the intestinal endothelium. This leakage into the blood may promote systemic inflammation known to contribute to the pathogenesis of diabetic retinopathy. These data suggested a loss of the protective arm of RAS contributes to the impairment of HSPCs and alteration of gut microbiota, both of which may contribute to the development of diabetic retinopathy.
This is the first book addressing in full the most important aspects of the angiotensin-(1-7), the key peptide of the protective axis and the main component in the new modulatory concept of the renin-angiotensin system. It features a detailed review of angiotensin-(1-7) and its receptor Mas, comprising the historical background, enzymatic pathways for generation, functions, integrative aspects of its protective profile, and its therapeutic potential. It also encompasses a comprehensive presentation of current knowledge about its widespread biological actions on several tissues, as well as the most recent scientific achievements, emerging from preclinical and clinical trials. Dr. Santos is a renowned researcher on the Renin-Angiontensin system, with remarkable achievements regarding the role of peptides such as alamandine and angiontensin-(1-7). He has also worked on the potential clinical applicability of angiotensin-(1-7)-related drugs for cardiovascular diseases. He has an extensive publication record in the field, including the publication of the book The Protective Arm of the Renin Angiotensin System (Academic Press, 2015). Angiotensin-(1-7) will make a unique contribution to the literature and will be an important resource for biomedical students and researchers, medical practitioners and any other professional interested in this peptide and its role in the renin-angiotensin system.
This book of the series on “Advances in Biochemistry in Health and Disease” includes state-of-the-art information on the status of renin-angiotensin system (RAS) in the form of 24 chapters. This book has been organized into three sections: (i) General Implications of RAS in human health and Infectious Diseases, (ii) Lung, Liver and Kidney Diseases, and (iii) Development of Cancer. Each chapter has discussed comprehensive knowledge regarding the molecular and cellular aspects of the role of RAS in the pathophysiology and pharmacotherapy of different disease processes. Biochemical mechanisms associated with angiotensin II type 1 and type II receptors, and angiotensin (1-7) MAS receptors for the occurrence of both harmful and beneficial effects of prolonged activation of RAS in different diseases have been outlined. It is noteworthy to point out that different chapter in this book were prepared by recognized global expertise in the area of inflammation, oxidative stress and signal transduction pathways to highlight the role of RAS in different diseases. It is our sincere hope that this book will be of great interest to both biomedical investigators and health professionals as well as graduate students and postdoctoral fellows all over the world.
Until recently, the renin-angiotensin-aldosterone system has been considered a systemic endocrine hormonal system exclusively. It is now known that each component of the renin-angiotensin system is produced, synthesized and indeed, present in many organisms including the heart and vessels. This volume presents the most recent clinical and laboratory experiences of the leading physicians and investigators in the field of the local cardiac renin-angiotensin aldosterone system. Cardiovascular, renal and hypertension oriented physicians, investigators and scientists would find this book of interest. Edward D. Frohlich, M.D., M.A.C.P, F.A.C.C., is the Alton Ochsner Distinguished Scientist at the Ochsner Clinic Foundation in New Orleans, Louisiana. He is also Professor of Medicine and of Physiology at Louisiana State University School of Medicine, New Orleans, and Clinical Professor of Medicine and Adjunct Professor of Pharmacology at Tulane University School of Medicine, New Orleans. He is past Editor-in-Chief of the American Heart Association journal HYPERTENSION. Richard N. Re, M.D., is the Section Head, Hypertension at the Ochsner Clinic Foundation in New Orleans, Louisiana. He is also Ochsner's Scientific Director of Research.
Selected Chapters from the Renin-Angiotensin System aims to provide a comprehensive overview of the most important physiological and pathophysiological roles of the renin-angiotensin system (RAS). The complex and convoluted RAS has been investigated for many years and, through rigorous scientific research, many important and previously unknown components and functions of the RAS have come to light. These discoveries have been crucial in the understanding of this system and provide a basis for effective modulation of the system as part of therapeutic strategies for a number of widespread disorders. New studies are continuing to elucidate the RAS and the mechanisms associated with its functions. This book discusses relevant scientific knowledge about the RAS and intends to introduce the reader to cutting-edge research with an accentuation on the mechanisms at the functional/physiological and molecular/cellular levels.
Exploring the contractile activity of smooth muscle segments isolated from various organs of healthy animals and animals with experimentally induced diabetes, she obtained original data about angiotensin II-induced force and time parameters. For the first time, she established the effect of ghrelin on angiotensin II-provoked contraction of the urinary bladder. Original data on the role of both types of angiotensin receptors for the contractile activity of the various segments of the gastrointestinal tract and bladder were obtained. By applying specific software for force and time parameter analysis, the contribution of different types of angiotensin receptors on muscle contractility has been shown. The new methodology was used to analyze the data obtained during the registration of smooth muscle relaxation activity, which allows the determination of not only the magnitude of the mechanical response but also the parameters related to the time and speed of the contractions. Plasma renin activity models have been developed using mathematical approaches to predict the effect of different drug doses on the behavior of the system.
The primary aim of this book is to provide a topical and timely forum for the critical appraisal of an area of renin-angiotensin system (RAS) research that is expanding rapidly. In this respect, a collection of thirteen chapters from distinguished and world-class experts in the field has been presented on the contemporary research of the RAS and their implications in human disease. This book is an indispensable tool tailor-made for specialists, non-specialists and the novice.
This book is an open access dissemination of the EU COST Action ADMIRE in Aldosterone/Mineralocorticoid Receptor (MR) physiology and pathophysiology. Aldosterone is the major hormone regulating blood pressure. Alterations in blood levels of aldosterone and genetic mutations in the MR receptor are major causes of hypertension and comorbidities. Many of the drugs in clinical use, and in development for treating hypertension, target aldosterone and MR actions in the kidney and cardiovascular system. The ADMIRE book assembles review chapters from 16 European ADMIRE laboratories providing the latest insights into mechanisms of aldosterone synthesis/secretion, aldosterone/MR physiology and signaling, and the pathophysiological roles of aldosterone/MR activation.
The renin-angiotensin system (RAS) is a major hormonal system that plays an essential role in regulating salt-water balance and blood pressure. In this book, the authors discuss the physiology, role in disease and health implications of RAS. Topics include the function of the renin-angiotension-aldosterone system in ISIAH rats with stress-sensitive arterial hypertension; RAS implications for eye diseases, obesity and diabetes, and cardiovascular disease; intensive blockade of renin-angiotensin systems; glomerular renin-angiotensin system activation; the role of vitamin D in RAS; the renin-angiotensin system in the pathogenesis of intracranial aneurysms; and a discussion on whether angiotensin-converting enzyme inhibitors are a contradiction for contrast-induced nephropathy prophylaxis?