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Carotid body function in heart failure.

Harold D Schultz1, Yu Long Li

  • 1Department of Cellular and Integrative Physiology, University of Nebraska College of Medicine, 985850 Nebraska Medical Center, Omaha, NE 68198-5850, USA. hschultz@unmc.edu

Respiratory Physiology & Neurobiology
|March 22, 2007
PubMed
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The carotid body (CB) chemoreflex is enhanced in chronic heart failure (CHF), increasing sympathetic nerve activity (SNA). This involves altered signaling in the CB and central nervous system (CNS), with angiotensin II and nitric oxide playing key roles.

Area of Science:

  • Cardiovascular Physiology
  • Neuroscience
  • Renal Physiology

Background:

  • Chronic heart failure (CHF) is associated with elevated sympathetic nerve activity (SNA).
  • The carotid body (CB) chemoreflex is implicated in regulating SNA.
  • Understanding the CB's role in CHF is crucial for therapeutic development.

Purpose of the Study:

  • To review the functional characteristics of the CB chemoreflex in controlling SNA in CHF.
  • To elucidate the mechanisms underlying enhanced CB chemoreflex activity in CHF.
  • To identify the roles of specific signaling pathways in the CB and CNS.

Main Methods:

  • Review of existing literature on CB chemoreflex in CHF.
  • Analysis of evidence from both human patients and animal models of CHF.

Related Experiment Videos

  • Examination of cellular and molecular mechanisms within the CB and CNS.

    • Main Results:

    • The CB chemoreflex is enhanced in CHF, contributing to elevated SNA.
    • Altered afferent discharge and ion channel function (K+ currents) in CB glomus cells.
    • Downregulation of nitric oxide synthase (NOS)/NO and upregulation of angiotensin II (Ang II)/AT1R signaling in CB glomus cells.
    • Central nervous system (CNS) interactions, including altered baroreceptor input and central Ang II, further increase sympathetic drive.
    • Impaired NO function in the hypothalamus contributes to enhanced SNA.

    Conclusions:

    • The enhanced CB chemoreflex in CHF is a multi-faceted adaptation.
    • Both the CB and CNS exhibit altered signaling, involving Ang II and NO.
    • These complementary mechanisms aim to increase CB chemoreflex function in CHF.