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Ca2+ Signaling and Heart Rhythm

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198740 Year: Pages: 133 DOI: 10.3389/978-2-88919-874-0 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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Abstract

Ca2+ is a key second messenger in the intricate workings of the heart. In cardiac myocytes, Ca2+ signaling controls or modulates electrophysiological function, excitation-contraction coupling, contractile function, energy balance, cell death, and gene transcription. Thus, diverse Ca2+-dependent regulatory processes occur simultaneously within a cell. Yet, distinct signals can be resolved by local Ca2+ sensitive protein complexes and differential Ca2+ signal integration. In addition to its importance to normal cardiac function, such regulation is also crucial in disease conditions. Ca2+ is likely involved in ectopic cardiac rhythms in both atrial and ventricular tissues through generating triggered activity often appearing as delayed afterdepolarisations, particularly following cellular Ca overloading. Recent studies also implicate Ca2+ in Na+ channel expression and properties with consequences for conduction velocity and therefore arrhythmic substrate. At the cellular level, such regulation involves control of the activity of membrane ion channels and Ca2+ handling proteins. These in turn involve multiple extra- and intracellular signaling pathways. This e-book assembles review and original articles from experts in this field. It summarises major recent progress bearing on roles of Ca2+ in cardiac electrophysiological function encompassing both normal and abnormal cardiac function. These extend from physiological roles of Ca2+ signaling in pacemaker function, in particular generation of sino-atrial pacemaker potentials, to pathological roles of abnormal Ca2+ signaling in both atrial and ventricular arrhythmogenesis. It also seeks to bridge the gap between advances in basic science and development of new therapies.

Keywords

Ca2+ --- Heart --- Pak1 --- SA node --- voltage gated Ca2+ channels --- TRPC --- STIM1 --- Orai1 --- PP2A

Dysregulation of Autonomic Cardiac Control by Traumatic Stress and Anxiety

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199150 Year: Pages: 118 DOI: 10.3389/978-2-88919-915-0 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Psychology
Added to DOAB on : 2016-01-19 14:05:46
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Current understanding of the interplay between sympathetic and parasympathetic influences on cardiac response to environmental stimuli and subsequent response selection (e.g. maintenance of resting homeostasis, mobilization of defensive response, task performance, tonic immobilization, and/or affiliation) will be explored. Reference will be made to how these processes conjoin with proposed polyvagal theory. Cardiac adjustments to environmental stimuli affect the internal physiological state of the organism as well as the quality of information processing that the individual can perform during the stimulus appraisal stage of the orienting response. Bradyrdia is adaptive in early stages of orientation to novel or potential threat, while greater HRV power serves to facilitate self-regulation, stimulus information processing and appraisal, and appropriate response selection. This issue is devoted to current research findings on how normal patterns of cardiac autonomic regulation of HRV are disrupted in PTSD, impairing sustained attention to the environment and increasing the rate of inappropriate responding to stimuli. Origins of our current state of understanding in the ‘intake-rejection’ hypothesis will be considered, and how the intake-rejection hypothesis has morphed into present-day Optimal Performance practice. Additionally, empirical data where available will be presented on how dysregulation of the normal pattern of cardiac autonomic regulation by PTSD impairs sustained attention to the environment, and increases the rate of inappropriate responding to stimuli through disinhibition, poor impulse control, emotional withdrawal, over-arousal, and attentional bias. Current research findings are sought that address in controlled, experimental and clinical trials the restorative effects of HRV biofeedback on HRV power, and how increases in HRV power relate to improved attention / immediate memory and self-regulation of affect using outcome measures of cognition, symptoms of PTSD and depression, stress perception, and level of adaptive function.

Carotid Body: A New Target for Rescuing Neural Control of Cardiorespiratory Balance in Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199433 Year: Pages: 134 DOI: 10.3389/978-2-88919-943-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
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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.

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