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Altered effects of potassium channel modulation in the coronary circulation in experimental hypercholesterolemia

V Mathew1, A Lerman

  • 1Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. mathew.verghese@mayo.edu

Atherosclerosis
|February 13, 2001
PubMed

Insights

Hypercholesterolemia enhances coronary potassium channel function, leading to altered coronary blood flow regulation. This highlights the critical role of potassium channels in managing coronary vasomotor tone during disease.

Area of Science:

  • Cardiovascular Physiology
  • Pharmacology
  • Pathophysiology

Background:

  • Potassium (K(+)) channels are crucial for regulating coronary blood flow.
  • Experimental hypercholesterolemia is known to alter coronary vasomotion.
  • The specific role of K(+) channels in hypercholesterolemia-induced changes in coronary blood flow was previously unevaluated.

Purpose of the Study:

  • To investigate the role of potassium channels in regulating coronary hemodynamics in a model of experimental hypercholesterolemia.
  • To assess the impact of hypercholesterolemia on the coronary vasomotor response to specific potassium channel modulators.

Main Methods:

  • Infusion of pinacidil (K(+) channel opener), glibenclamide (K(+) channel blocker), and N-monomethyl-L-arginine (L-NMMA, nitric oxide synthase inhibitor) into the left anterior descending artery of pigs.
  • Comparison of responses before and after 10 weeks of a 2% cholesterol diet.
  • Measurement of coronary blood flow (CBF) and coronary artery diameter (CAD).

Main Results:

  • Intracoronary pinacidil significantly increased CBF and CAD in hypercholesterolemic pigs compared to normolipidemic controls.
  • Intracoronary glibenclamide significantly decreased CBF and CAD in hypercholesterolemic pigs compared to controls.
  • The effect of intracoronary L-NMMA on CBF and CAD was significantly attenuated in hypercholesterolemic pigs.
  • L-NMMA pretreatment did not affect the pinacidil response in normal pigs.

Conclusions:

  • Experimental hypercholesterolemia enhances the functional effects of coronary potassium channel modulation.
  • Basal nitric oxide activity is attenuated in experimental hypercholesterolemia, but this alone does not explain the enhanced potassium channel effects.
  • The potassium channel pathway is critically important for regulating coronary vasomotor tone in pathophysiological conditions like hypercholesterolemia.
Abstract

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