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Role of blood flow in carotid body chemoreflex function in heart failure

Yanfeng Ding1, Yu-Long Li, Harold D Schultz

  • 1Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA.

The Journal of Physiology
|November 17, 2010
PubMed

Insights

Reduced blood flow to the carotid body (CB) increases peripheral chemoreflex sensitivity in chronic heart failure (CHF). This study shows reduced blood flow to the CB potentiates chemoreflex function in rabbits.

Area of Science:

  • Cardiovascular Physiology
  • Respiratory Control
  • Renal Physiology

Background:

  • Peripheral chemoreflex sensitivity is heightened in chronic heart failure (CHF).
  • Reduced tissue blood supply is characteristic of CHF, but its role in potentiating chemoreflex sensitivity is unclear.
  • The carotid body (CB) is a key peripheral chemoreceptor sensitive to oxygen and carbon dioxide levels.

Purpose of the Study:

  • To investigate the impact of chronically reduced blood flow to the carotid body (CB) on peripheral chemoreflex function.
  • To determine if reduced CB blood supply contributes to enhanced chemoreflex sensitivity observed in chronic heart failure (CHF).

Main Methods:

  • Pacing-induced chronic heart failure (CHF) model and carotid artery occlusion (CAO) model in rabbits.
  • Measurement of carotid artery blood flow and CB blood supply using fluorescent microspheres.
  • Assessment of in vivo peripheral chemoreflex sensitivity, isolated CB chemoreceptor activity, and potassium currents in CB glomus cells.
  • Analysis of neural nitric oxide synthase (nNOS), nitric oxide (NO) levels, angiotensin II (Ang II) type 1 receptor (AT1-R) expression, and Ang II concentration in CB tissue.

Main Results:

  • Both CHF and CAO models demonstrated significantly reduced CB blood supply.
  • Carotid artery occlusion (CAO) enhanced peripheral chemoreflex sensitivity, increased CB chemoreceptor activity, and decreased outward potassium current (Ik) in CB glomus cells.
  • CAO led to suppressed nNOS expression and NO levels, with elevated AT1-R protein and Ang II concentration in the CB, mirroring changes seen in CHF rabbits.
  • A nitric oxide (NO) donor and an AT1-R antagonist successfully reversed the CAO-induced enhancement of chemoreflex sensitivity.

Conclusions:

  • Reduced blood flow to the carotid body (CB) is a significant factor in augmenting peripheral chemoreflex sensitivity.
  • The observed changes in nNOS, NO, AT1-R, and Ang II in the CB play a role in this flow-dependent chemoreflex potentiation.
  • These findings suggest that impaired CB blood supply contributes to the heightened chemoreflex sensitivity in chronic heart failure (CHF).

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