The renin-angiotensin system (RAS) is one of the most important endocrine (tissue-to-tissue), paracrine (cell-to-cell) and intracrine (intracellular/nuclear) humoral systems in the regulation of blood pressure, cardiovascular, and kidney function in health and disease. The RAS has remarkably evolved from the initial discovery of the rate-limiting enzyme renin to a complex biochemical and physiological cascade involving more than a dozen members. Currently, there are up to five axes or pathways identified in the RAS; each has its substrate, enzyme, effector peptide, receptor, and downstream signaling pathways. These include the renin/ACE/ANG II/AT1 receptor, the APA/ANG III/AT2 receptor, the ACE2/ANG (1-7)/Mas receptor, the prorenin/prorenin receptor (PRR), and the ANG IV/AT4 receptor (IRAP) pathways. Accordingly, the roles of the RAS have expanded well beyond the classic endocrine paradigm as a powerful vasoconstrictor, a potent aldosterone stimulator, or a sodium-retaining hormonal system. The goals of this article are to review and discuss the current insights into and new perspectives on the expression, localization, and novel actions of the RAS with a focus in the kidney. Special emphasis will be placed on recently discovered new members of the RAS derived from studies using innovative mutant rats or mice that either overexpress (knockin) or are deficient (knockout) of a particular substrate, enzyme, ANG peptide, or receptor. This new knowledge will help improve our understanding how each of these pathways act directly or indirectly to regulate blood pressure, cardiovascular and kidney function in physiology, and can be targeted to treat hypertension, cardiovascular and renal diseases.

The Textbook of Nephro-Endocrinology is the definitive translational reference in the field of nephro-endocrinology, investigating both the endocrine functions of the kidneys and how the kidney acts as a target for hormones from other organ systems. It offers researchers and clinicians expert, gold-standard analyses of nephro-endocrine research and translation into the treatment of diseases such as anemia, chronic kidney disease (CKD), rickets, osteoporosis, and, hypoparathyroidism. Investigates both the endocrine functions of the kidneys and how the kidney acts as a target for hormones from other organ systems Presents a uniquely comprehensive and cross-disciplinary look at all aspects of nephro-endocrine disorders in one reference work Clear translational presentations by the top endocrinologists and nephrologists in each specific hormone or functional/systems field

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.

The renin-angiotensin system (RAS) has long been seen as a systemic endocrine system in which angiotensin II (ANG II) is solely involved in blood pressure regulation and the mediation of aldosterone release. However, it is now known that specific organ systems exhibit their own local RAS, functioning for the most part independently from their systemic counterpart. A deluge of data from the last decade has shown that ANG II displays many more functions than just regulating blood pressure: ANG II is a growth factor, exhibits profibrogenic actions, and even serves as a proinflammatory cytokine. It is now clear that this peptide plays a pivotal role in the progression of chronic kidney disease towards endstage renal failure. Clinical studies have provided compelling evidence that interference with ANG II slows this deterioration of renal function.This publication presents the first comprehensive summary of this important topic: Basic concepts as well as clinical aspects of the RAS are reviewed by international experts who made many of the key discoveries that constitute our contemporary understanding of ANG II as a central factor in the progression of renal disease. This publication should be read by physicians treating patients with chronic renal diseases (internists, nephrologists and urologists). Moreover, basic scientists such as renal physiologists, renal pathologists and biochemists who want a comprehensive overview of the subject will profit from reading this book.

The Renin-Angiotensin Aldosterone System (RAAS) plays an important role not only in salt and water homeostasis but also in the cardiovascular system, the kidney, and the brain. While several volumes address different aspects of the RAAS function, this book provides cutting-edge information on the pathogenesis of various disorders related to RAAS overactivation. It also presents unique aspects of RAAS functioning that have not been sufficiently described in the literature. Topics covered include assessment of hypoaldosteronism in infancy, RASS and cognitive decline, and the role of RAAS in the pathogenesis of COVID-19. Written by experts in the field in an easy-to-follow and illustrated format, this volume will benefit students and practitioners, as well as clinical and basic science investigators alike.

Chronic kidney disease is one of the world's major public health problems, and the prevalence of kidney failure is rising steadily. Among the risk factors for a faster progression of renal disease are hypertension and proteinuria, many studies clearly demonstrating that hypertension is both a cause and consequence of chronic kidney disease. Namely, renal blood pressure regulation seems to be involved in five major pathophysiological mechanisms (all closely related to the renin-angiotensin system): Pressure-natriuresis, renal sympathetic nervous system, renal blood flow, intraglomerular pressure and tubuloglomerular feedback. This book reviews experimental data which form the basis of our current understanding of the association between hypertension and kidney diseases: The pathogenesis of increased blood pressure, the mechanisms by which systemic hypertension promotes progressive kidney failure, and the impact of antihypertensive agents on experimental renal mechanisms involved in hypertension. Furthermore, the role of angiotensin II receptor blockers in both the control of systemic blood pressure and the reduction of proteinuria is examined in an attempt to define optimal therapeutic strategies to prevent the otherwise inexorable deterioration of renal function in patients with chronic kidney disease.

The renin-angiotensin system (RAS) is a hormonal system that is responsible for regulating plasma sodium ion concentration and arterial blood pressure in the body. The system involves several peptides such as angiotensin I and II as well as angiotensin converting enzyme (ACE) to enable the constriction of arterial blood vessels in the lung. Angiotensin II also stimulates the production of the hormone aldosterone in the kidneys which brings sodium ions into the bloodstream in exchange for potassium ions. Malfunctions of the RAS can lead to hypertension, heart failure, diabetes and renal complications. Thus the biochemical components of this system serve as important targets for therapeutic drugs. This monograph is a compilation of updated reviews on the RAS. The monograph covers describes the components of the system to explaining its physiological and clinical features in the cardiovascular system and the kidneys. This is followed by sections explaining the biochemistry of the RAS system in cardiovascular and renal disease and the pharmacology of relevant therapeutic drugs. Additional information on the effect of exercise states and methods to quantify angiotensins for molecular diagnosis is also presented in the concluding sections. Information in the monograph will be of interest to physiologists and endocrinologists involved in medical studies or clinical practice. Readers will be able to understand the RAS with a holistic frame of reference.