作者: M. D. Thames , M. E. Dibner-Dunlap
DOI: 10.1007/978-3-642-76366-3_11
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摘要: It has been known for many years that clinical congestive heart failure is accompanied by a neurohumoral excitatory state characterized increased levels of norepinephrine and muscle sympathetic nerve activity, plasma renin vasopressin circulating angiotensin II, aldosterone. These mechanisms augment peripheral vasoconstriction sodium retention the kidney are hallmarks failure. A similar can be provoked in normal animals following acute interruption sensory input from arterial baroreceptors cardiac receptors with afferent vagal fibers [1]. We have previously suggested could result part baroreflex abnormalities which may present [2]. If this so, then it possible such limb these reflexes, CNS, or neuroeffector mechanisms. Whether not baroreflexes play an important causal role development rate, reflexes still terms interfering adaptive dealing cardiovascular stresses to humans normally exposed. For example, exercise emotion produce sympathoexcitation, tachycardia, hypertension, modulated