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Effect of ATP-sensitive potassium channel inhibition on coronary metabolic vasodilation in humans

H M Omar Farouque1, Stephen G Worthley, Ian T Meredith

  • 1Cardiovascular Research Centre, Monash Medical Centre and Monash University, Melbourne, Australia.

Arteriosclerosis, Thrombosis, and Vascular Biology
|March 16, 2004
PubMed

Insights

ATP-sensitive potassium (K(ATP)) channels regulate coronary blood flow. Inhibiting these channels reduced metabolic vasodilation in human coronary arteries, indicating their role in hyperemia.

Area of Science:

  • Cardiovascular Physiology
  • Vascular Biology
  • Potassium Channel Function

Background:

  • ATP-sensitive potassium (K(ATP)) channels are known to influence coronary blood flow (CBF).
  • The specific role of K(ATP) channels in human coronary metabolic vasodilation remains unclear.

Purpose of the Study:

  • To investigate the contribution of vascular K(ATP) channels to human coronary metabolic vasodilation.
  • To assess the effect of K(ATP) channel inhibition on coronary hemodynamics during metabolic stimulation.

Main Methods:

  • Seventeen patients underwent assessment of coronary hemodynamics.
  • K(ATP) channels were inhibited using intracoronary glibenclamide.
  • Metabolic vasodilation was induced by rapid right ventricular pacing, with coronary blood velocity measured by Doppler guidewire.

Main Results:

  • Glibenclamide reduced resting coronary blood flow and increased resting coronary vascular resistance.
  • K(ATP) channel inhibition significantly blunted pacing-induced hyperemia, reducing peak CBF and increasing minimum CVR.
  • The total hyperemic volume, estimated by the area under the flow-versus-time curve, was also reduced by glibenclamide.

Conclusions:

  • Vascular K(ATP) channels play a significant role in the regulation of human coronary blood flow.
  • These channels are involved in the functional coronary hyperemia response following metabolic stimulation.
Abstract

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