Background

Most of us are unaware when the ANS is at work. Its functions are involuntary and reflexive, such as changing the size of blood vessels or causing our hearts to beat faster. Scientists are well aware that autonomic dysfunction contributes to progression of heart failure. The most effective treatments for heart failure specifically target the peripheral manifestations of neurohumoral (nerve transmission) activation. Yet the understanding of the mechanisms leading to neurohumoral excitation in heart failure is still quite limited.

Over the last several decades, substantial evidence has been amassed to support the concept that peripheral nerve fibers connecting the heart and vascular tree to the central nervous system are altered in heart failure. Dysfunction has been described in all components of the reflexes mediated by these cardiovascular afferent systems the afferent fibers themselves, the central processing of the afferent signals, the nerves signals away from the heart, and the key organs themselves. In general, the influence of low- and high-pressure baroreceptors that normally restrain sympathetic drive and vasopressin release is diminished, whereas the excitatory influences of arterial chemoreceptors and cardiac sympathetic afferent fibers are enhanced.

Central nervous system (CNS) neurons affecting cardiovascular regulation respond to humoral (carried by blood) as well neural signals. Blood-borne neuroactive peptides, too large to readily cross the blood-brain barrier, may influence the brain by activating sensory neurons at specific sites in hindbrain and forebrain that lack a blood-brain barrier or b
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
18-Mar-2003