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

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 pressure 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

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. Under normal conditions, the renal mechanosensory nerves activated by stretch 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.

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. Under normal conditions, the renal mechanosensory nerves activated by stretch 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.

Now in paperback, the second edition of the Oxford Textbook of Critical Care is a comprehensive multi-disciplinary text covering all aspects of adult intensive care management. Uniquely this text takes a problem-orientated approach providing a key resource for daily clinical issues in the intensive care unit. The text is organized into short topics allowing readers to rapidly access authoritative information on specific clinical problems. Each topic refers to basic physiological principles and provides up-to-date treatment advice supported by references to the most vital literature. Where international differences exist in clinical practice, authors cover alternative views. Key messages summarise each topic in order to aid quick review and decision making. Edited and written by an international group of recognized experts from many disciplines, the second edition of the Oxford Textbook of Critical Careprovides an up-to-date reference that is relevant for intensive care units and emergency departments globally. This volume is the definitive text for all health care providers, including physicians, nurses, respiratory therapists, and other allied health professionals who take care of critically ill patients.

Reflex Control of the Circulation presents an interdisciplinary discussion of concepts in the reflex control of circulation. This volume describes aspects of autonomic receptor physiology, central pathways of reflex control, the electrophysiology of cardiovascular afferents, the interaction between reflexes, the autonomic control of regional blood flows, the autonomic control of fluid and electrolyte balance, and neurohumoral control of the circulation through normal and pathological states (e.g., hypertension, congestive heart failure). In addition, the regulation of regional blood flow during exercise and developmental aspects of reflex control are examined. Any researcher interested in the autonomic system and its role in circulation will find this book fascinating reading.

This book presents up-to-date information on the clinical-pathophysiological features of acute renal injury and discusses the KDIGO diagnostic criteria, as well as novel experimental findings, including in the area of regenerative medicine. It also highlights the clinical-pathophysiological importance of AKI in clinical settings, including differential diagnoses and management of AKI. In the past, the pathology associated with sudden renal impairment was characterized as acute renal failure (ARF). However, in the 2000s, the joint efforts of specialists in fields including nephrology, intensive care medicine, and cardiovascular medicine led to the introduction of a novel concept known as acute kidney injury (AKI). As medical care progressed, patients such as high-risk elderly subjects who were not deemed to be candidates for invasive therapy came to be treated in intensive care units (ICUs). As a result, kidney injury as a subset of multiple organ failure was re-considered as AKI, especially in intensive care medicine. AKI was then proposed as a novel disease concept to emphasize the importance of early diagnosis and early intervention to improve prognosis.Presenting novel features, such as the definition of AKI, risk factors and management; biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL) and L-type fatty acid-binding protein (L-FABP); long-term outcomes of AKI; as well as renal regeneration using iPS cell, manipulation of embryonic genes, and Xenotransplanted embryonic kidney, this book is of interest to all physicians and researchers in this field around the globe.

This book introduce neurourology as an emerging interdisciplinary area that covers the basic and clinical studies of the neural control on the normal lower urinary tract and the lower/upper urinary tract dysfunction due to neuropathy disorders. It systematically describes all aspects of neurourology from the epidemiology of the neurogenic bladder; to the pathology and pathophysiology of the lower urinary tract; to the diagnosis and treatment of the neurogenic bladder by conservative therapies or surgeries. This book provides a useful resource for medical doctors, nurses and students in the field of neurourological conditions. All the topics are written by internationally recognized specialists in their field.