Stress, catecholamines, and cardiovascular disease
Stress is an integral part of life. But what is it, how does it affect the body, and what roles do stress and catecholamines play in acute and chronic manifestations of cardiovascular diseases? This book provides a comprehensive, science-based analysis of these issues. Scientific medicine attempts to explain diseases in terms of theories that observation or experimentation can test. The starting point for understanding the roles of stress and catecholamines in cardiovascular disorders is a theory defining stress. This book presents a new homeostatic theory of stress and distress and applies this theory to explain the important roles of endogenous catecholamines--norepinephrine, epinephrine, and dopamine--and other effector systems in maintaining the internal environment during stress. The theory proposes coordinated activation of the body's several stress systems in primitively specific patterns during exposure to various stressors. Comparator "homeostats" interpret afferent information about specific physiological or chemical monitored variables and regulate the operations of effector systems. Via a hierarchical mosaic of central neural cell clusters, the brain constantly redefines homeostasis by resetting homeostats, especially during stress. The presentation summarizes difficult and complex literature about central neural mechanisms participating in sympathoadrenal responses to stress and analyzes theories about the roles of catecholamines in the brain. Clinical methods to assess sympathoadrenal activity are described, including the latest tracer-kinetic and nuclear scanning techniques. The possibly pathophysiologic effects of the derangement of catecholaminergic function in cardiovascular diseases receive particular attention. Attempting to separate fact from opinion, the book considers objectively several prevalent and controversial theories -inking stress and cardiovascular disease. The book concludes with the proposal of a new discipline in clinical medicine: neurocardiology.
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Stress and Science
The Fact of Organization
Peripheral Catecholaminergic Systems
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a2-adrenoceptors ACTH acute adrenal adrenergic adrenoceptors adrenomedullary afferent agonists arterial augments autonomic baroreceptor baroreflex behavior blockade blood pressure brain brainstem Cannon cardiovascular carotid sinus catechol catecholaminergic catecholamines cells central neural circulating Clin clinical clonidine concentrations coronary decreases DHPG disease distress DOPA DOPAC dopamine effector effects Eisenhofer elicit emotional endogenous EPI levels epinephrine Esler essential hypertension evokes excretion function Goldstein DS heart failure heart rate homeostatic hormone humans hypotension hypothalamus increases plasma inhibition innervation locus coeruleus mechanisms mediated medulla metabolism myocardial myocardial infarction nerve activity nervous system neuroendocrine neurons neurotransmitter noradrenergic norepinephrine nucleus orthostasis pathways patients patterns Pharmacol pheochromocytoma Physiol physiological plasma plasma catecholamine plasma levels plasma NE levels produces receptors reflexive regional regulation release renal RVLM Selye SHRs skeletal muscle spillover spinal stimulation stress responses stressors sympathetic activity sympathetic nerve sympathetic outflow sympathoneural activity syndrome uptake Uptake-1 urinary vagal vascular vasoconstriction vasodilation vasopressin venous ventricular yohimbine