The special issue of Molecular and Cellular Biochemistry focuses on `Control of Gene Expression by Catecholamines and the Renin-Angiotensin System' in health and disease. In recent years, great progress has been made in the understanding of catecholamine and angiotensin II modulated gene expression. There is also increasing evidence that catecholamine and angiotensin II induced cellular injury not solely arises from classical pathways but also from a perturbed gene expression. Taking into account that catecholamines and angiotensin II are vital for a balanced gene expression of many cells, the intriguing possibility arises that various disease are initiated or aggravated by such an imbalance. Catecholamine and angiotensin II influences can be in excess arising from, for example, hypercaloric food intake or psychosocial stress. During early progression of heart failure, sympathetic activity and angiotensin II influences also become increased. Due to beta-adrenergic receptor downregulation, depressed catecholamine influences are expected in the final stage of heart failure. An imbalanced influence of catecholamines and angiotensin II on gene expression leads to disordered molecular structures of the cell and an impaired cell function. This focused issue is organized into chapters concentrating on catecholamines, angiotensin II, and the interaction between catecholamines and angiotensin II. Basic biochemical processes are covered in detail and the potential of these pathways for explaining chronic diseases associated with excess catecholamine and angiotensin II influences should become apparent. It is hoped that this focussed issue triggers novel research into the development of drugs that are targeted at diseases characterized by an imbalanced gene expression involving catecholamines and angiotensin II.

This volume provides comprehensive coverage of the current knowledge of the physiology of the endocrine system and hormone synthesis and release, transport, and action at the molecular and cellular levels. It presents essential as well as in-depth information of value to both medical students and specialists in Endocrinology, Gynecology, Pediatrics, and Internal Medicine. Although it is well established that the endocrine system regulates essential functions involved in growth, reproduction, and homeostasis, it is increasingly being recognized that this complex regulatory system comprises not only hormones secreted by the classic endocrine glands but also hormones and regulatory factors produced by many organs, and involves extensive crosstalk with the neural and immune system. At the same time, our knowledge of the molecular basis of hormone action has greatly improved. Understanding this complexity of endocrine physiology is crucial to prevent endocrine disorders, to improve the sensitivity of our diagnostic tools, and to provide the rationale for pharmacological, immunological, or genetic interventions. It is such understanding that this book is designed to foster.

The kidney is innervated with efferent sympathetic nerve fibers reaching the renal vasculature, the tubules, the juxtaglomerular granular cells, and the renal pelvic wall. The renal sensory nerves are mainly found in the renal pelvic wall. Increases in efferent renal sympathetic nerve activity reduce renal blood flow and urinary sodium excretion by activation of α1-adrenoceptors and increase renin secretion rate by activation of β1-adrenoceptors. In response to normal physiological stimulation, changes in efferent renal sympathetic nerve activity contribute importantly to homeostatic regulation of sodium and water balance. The renal mechanosensory nerves are activated by stretch of the renal pelvic tissue produced by increases in renal pelvic tissue of a magnitude that may occur during increased urine flow rate. Activation of the sensory nerves elicits an inhibitory renorenal reflex response consisting of decreases in efferent renal sympathetic nerve activity leading to natriuresis. Increasing efferent sympathetic nerve activity increases afferent renal nerve activity which, in turn, decreases efferent renal sympathetic nerve activity by activation of the renorenal reflexes. Thus, activation of the afferent renal nerves buffers changes in efferent renal sympathetic nerve activity in the overall goal of maintaining sodium balance. In pathological conditions of sodium retention, impairment of the inhibitory renorenal reflexes contributes to an inappropriately increased efferent renal sympathetic nerve activity in the presence of sodium retention. In states of renal disease or injury, there is a shift from inhibitory to excitatory reflexes originating in the kidney. Studies in essential hypertensive patients have shown that renal denervation results in long-term reduction in arterial pressure, suggesting an important role for the efferent and afferent renal nerves in hypertension. Table of Contents: Part I: Efferent Renal Sympathetic Nerves / Introduction / Neuroanatomy / Neural Control of Renal Hemodynamics / Neural Control of Renal Tubular Function / Neural Control of Renin Secretion Rate / Part II: Afferent Renal Sensory Nerves / Introduction / Neuroanatomy / Renorenal Reflexes / Mechanisms Involved in the Activation of Afferent Renal Sensory Nerves / Part III: Pathophysiological States / Efferent Renal Sympathetic Nerves / Afferent Renal Sensory Nerves / Conclusions / References

Over the past century, we have made great strides in reducing rates of disease and enhancing people's general health. Public health measures such as sanitation, improved hygiene, and vaccines; reduced hazards in the workplace; new drugs and clinical procedures; and, more recently, a growing understanding of the human genome have each played a role in extending the duration and raising the quality of human life. But research conducted over the past few decades shows us that this progress, much of which was based on investigating one causative factor at a time—often, through a single discipline or by a narrow range of practitioners—can only go so far. Genes, Behavior, and the Social Environment examines a number of well-described gene-environment interactions, reviews the state of the science in researching such interactions, and recommends priorities not only for research itself but also for its workforce, resource, and infrastructural needs.

Cellular and Molecular Biology of the Renin-Angiotensin System provides the first review and update of the state-of-the-art cellular and molecular aspects of the renin-angiotensin system. The book presents detailed analyses from world experts on each component of this system, including future directions. Topics range from angiotensin II receptor subtypes to processing of renin to the use of transgenic animal models for studying the role of this system in hypertension. Cellular and Molecular Biology of the Renin-Angiotensin System is essential reading for physiologists of the renin-angiotensin system, endocrinologists, cardiovascular specialists, renal physiologists, and neurobiologists.

This open access book presents a comprehensive overview of dilated cardiomyopathy, providing readers with practical guidelines for its clinical management. The first part of the book analyzes in detail the disease’s pathophysiology, its diagnostic work up as well as the prognostic stratification, and illustrates the role of genetics and gene-environment interaction. The second part presents current and future treatment options, highlighting the importance of long-term and individualized treatments and follow-up. Furthermore, it discusses open issues, such as the apparent healing phenomenon, the early prognosis of arrhythmic events or the use of genetic testing in clinical practice. Offering a multidisciplinary approach for optimizing the clinical management of DCM, this book is an invaluable aid not only for the clinical cardiologists, but for all physicians involved in the care of this challenging disease.

The special issue of Molecular and Cellular Biochemistry focuses on `Control of Gene Expression by Catecholamines and the Renin-Angiotensin System' in health and disease. In recent years, great progress has been made in the understanding of catecholamine and angiotensin II modulated gene expression. There is also increasing evidence that catecholamine and angiotensin II induced cellular injury not solely arises from classical pathways but also from a perturbed gene expression. Taking into account that catecholamines and angiotensin II are vital for a balanced gene expression of many cells, the intriguing possibility arises that various disease are initiated or aggravated by such an imbalance. Catecholamine and angiotensin II influences can be in excess arising from, for example, hypercaloric food intake or psychosocial stress. During early progression of heart failure, sympathetic activity and angiotensin II influences also become increased. Due to beta-adrenergic receptor downregulation, depressed catecholamine influences are expected in the final stage of heart failure. An imbalanced influence of catecholamines and angiotensin II on gene expression leads to disordered molecular structures of the cell and an impaired cell function. This focused issue is organized into chapters concentrating on catecholamines, angiotensin II, and the interaction between catecholamines and angiotensin II. Basic biochemical processes are covered in detail and the potential of these pathways for explaining chronic diseases associated with excess catecholamine and angiotensin II influences should become apparent. It is hoped that this focussed issue triggers novel research into the development of drugs that are targeted at diseases characterized by an imbalanced gene expression involving catecholamines and angiotensin II.