Abstract
Systolic heart failure is a feed-forward phenomenon with devastating consequences. Impaired cardiac function is the initiating event, but central nervous system mechanisms activated by persistent altered neural and humoral signals from the periphery play an important sustaining role. Animals with experimentally induced heart failure have neurochemical abnormalities in the brain that, when manipulated, profoundly affect sympathetic drive, volume regulation, and cardiac remodeling--critical determinants of outcome. This brief review explores recent studies that provide a strong rationale for the development of pharmaceutical agents that target central nervous system abnormalities in heart failure.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Aldosterone / metabolism
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Angiotensins / drug effects
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Angiotensins / metabolism
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Animals
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Blood-Brain Barrier
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Brain / drug effects*
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Brain / metabolism
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Brain / physiopathology*
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Cardiovascular Agents / pharmacology*
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Cardiovascular Agents / therapeutic use*
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Cell Communication
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Cytokines / metabolism
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Drug Carriers
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Drug Design
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Heart Failure, Systolic / drug therapy*
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Heart Failure, Systolic / metabolism
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Heart Failure, Systolic / physiopathology*
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Humans
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Inflammation / metabolism
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Sympathetic Nervous System / drug effects
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Sympathetic Nervous System / physiopathology*
Substances
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Angiotensins
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Cardiovascular Agents
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Cytokines
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Drug Carriers
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Aldosterone