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The carotid body (CB) is in charge of adjusting ventilatory and cardiovascular function during changes in arterial blood gases. Regardless this essential function, the CB has been implicated in the sensing of other physiological signals such as changes in blood flow and glucose levels. More important, malfunction of the CB chemoreceptors has been associated with the progression and deterioration of several disease states such as hypertension, heart failure, renal failure, insulin resistance, diabetes and sleep apnea. Although the mechanisms involved in the alterations of the CB function in pathophysiology are currently under intense research, the development of therapeutic approaches to restore normal CB chemoreflex function remains unsolved. Recent studies showing the effect of CB denervation in pathophysiology have unveiled a key role of these arterial chemoreceptors in the development of autonomic imbalance and respiratory disturbances, and suggest that targeting the CB could represent a novel strategy to improve disease outcome. Unfortunately, classical pharmacotherapy intended to normalize CB function may be hard to establish since several cellular pathways are involved in the CB dysfunction. Augmented levels of angiotensin II, endothelin-1, cytokines and free radicals along with decreases in nitric oxide had all been related to the CB dysfunction. Moreover, changes in expression of angiotensin receptors, nitric oxide synthases and cytokines that take place within the CB tissue in pathological states also contribute to the enhanced CB chemoreflex drive. It has been shown in heart failure, hypertension and obstructive sleep apnea that the CB becomes tonically hyper-reactive. During the progression of the disease this CB chemosensory facilitation process induces central nervous system plasticity. The altered autonomic-respiratory control leads to increased cardiorespiratory distress and the deterioration of the condition. The focus of this e-book will be to cover the role of the CB in pathophysiology and to provide new evidence of the pathways involved in the maladaptive potentiation of the CB chemoreflex function. In memory of Professor Mashiko Shirahata and Professor Constancio Gonzalez.

Hypertension --- Autonomic Function --- Sleep Apnea --- Insulin Resistance --- Heart Failure --- Sympathetic Nervous System --- Carotid Body

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What does it mean to be human? There are many theories of the evolution of human behavior which seek to explain how our brains evolved to support our unique abilities and personalities. Most of these have focused on the role of brain size or specific genetic adaptations of the brain. In contrast, in this text, Fred Previc presents a provocative theory that high levels of dopamine, the most widely studied neurotransmitter, account for all major aspects of modern human behavior. He further emphasizes the role of epigenetic rather than genetic factors in the rise of dopamine. Previc contrasts the great achievements of the dopaminergic mind with the harmful effects of rising dopamine levels in modern societies and concludes with a critical examination of whether the dopaminergic mind that has evolved in humans is still adaptive to the health of humans and to the planet in general.

Philosophy of nature --- Dopaminergic mechanisms. --- Brain --- Human evolution. --- Neuropsychology. --- Neurophysiology --- Psychophysiology --- Evolution (Biology) --- Physical anthropology --- Evolutionary psychology --- Human beings --- Sympathetic nervous system --- Evolution. --- Origin --- Health Sciences --- Psychiatry & Psychology

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"Noradrenergic Signaling and Astroglia integrates what is known about the active role of astroglia in the locus coeruleus-noradrenergic system and outlines the most recent advances in the field. It discusses the molecular mechanisms underlying norepinephrine-induced receptor activation in astroglia, cellular metabolism and CNS energy provision, in vitro, ex vivo, and in vivo models, gliosignalling and neuronal activity, and astroglial networks, gap junctions, and morphological plasticity. The book also addresses the role of astroglial adrenergic receptor activation in memory formation, cognition, regulation of sleep homeostasis, and lastly in neurological disorders, including trauma (cellular edema), neurodegeneration (Alzheimer's disease), and neuroinflammation (multiple sclerosis). Noradrenergic Signaling and Astroglia is a valuable source of new knowledge for a wide audience, including graduate students, post-doctoral fellows, and researchers in neuroscience, life sciences, and the biological and biomedical sciences"--

Neuropathology --- Central nervous system. --- Noradrenergic mechanisms. --- Central nervous system --- Molecular aspects. --- Nervous system, Central --- Nervous system --- Norepinephrinergic mechanisms --- Sympathetic nervous system --- Norepinephrine

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Cardiovascular diseases pose an enormous clinical challenge, remaining the most common cause of death in the world. β-adrenoceptors play an important role on cardiac, vascular and/or endothelial function at a cellular level with relevant applications in several cardiovascular diseases, such as heart failure and hypertension. G protein–coupled receptors (GPCRs), including β-adrenergic receptors, constitute the most ubiquitous superfamily of plasma membrane receptors and represent the single most important type of therapeutic drug target. Sympathetic nervous system hyperactivity, which characterizes several cardiovascular diseases, such as heart failure and hypertension, as well as physiological ageing, has been proved to exert in the long-term detrimental effects in a wide range of cardiovascular diseases. Acutely, sympathetic hyperactivity represents the response to an insult to the myocardium, aiming to compensate for decreased cardiac output. This process involves the activation of beta-adrenergic receptors by catecholamine with consequent heart rate and cardiac contractility increase. However, long-term exposure of the heart to elevated norepinephrine and epinephrine levels, originating from sympathetic nerve endings and chromaffin cells of the adrenal gland, results in further progressive deterioration in cardiac structure and function. At the molecular level, sustained sympathetic nervous system hyperactivity is responsible for several alterations including altered beta-adrenergic receptor signaling and function (down-regulation/desensitization). Moreover, the detrimental effects of catecholamine affect also the function of different cell types including, but not limited to, endothelial cells, fibroblasts and smooth muscle cells. Thus, the success of beta-blocker therapy is due, at least in part, to the protection of the heart and the vasculature from the noxious effects of augmented catecholamine levels. The current research topic aims to support the progress towards understanding the role of sympathetic nervous system under physiological conditions, and the contribution of its hyperactivity in the pathogenesis and progression of cardiovascular diseases. The topic is open to original studies, descriptions of new methodologies, reviews and opinions.

Cardiovascular system --- Cardiovascular system --- Cardiovascular system --- Diseases. --- Diseases --- Pathogenesis. --- Diseases --- Prevention --- Research. --- GRK2 --- Beta-adrenoceptors --- exercise training --- Heart Failure --- Sympathetic Nervous System --- beta-blockers --- functional recovery

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The field of autonomic neuroscience research concentrates on those neural pathways and processes that ultimately modulate parasympathetic and sympathetic output to alter peripheral organ function. In the following ebook, laboratories from across the field have contributed reviews and original research to summarize current views on the role of the brain in tuning peripheral organ performance to regulate body temperature, glucose homeostasis and blood pressure.

Disease control. --- Hypertension --- Nucleus Accumbens --- Thermogenesis --- vagal afferents --- TRPV Cation Channels --- Leptin --- Sympathetic Nervous System --- Parasympathetic Nervous System --- Glucose --- Hypoglycemia --- Disease management --- Clinical medicine --- Health services administration --- Medical care --- Decision making --- Cost control