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Isolation of Murine Coronary Vascular Smooth Muscle Cells
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Isolation of Murine Coronary Vascular Smooth Muscle Cells

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Downregulation of BK channel function and protein expression in coronary arteriolar smooth muscle cells of type 2

Tong Lu1, Qiang Chai1,2, Guoqing Jiao1,3

  • 1Department of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW., Rochester, Minnesota, USA.

Cardiovascular Research
|June 1, 2018
PubMed
Abstract

Insights

Type 2 diabetes impairs coronary microvascular function by altering large conductance calcium-activated potassium (BK) channels. This dysfunction involves reduced BK channel expression and function, impacting vasodilation in diabetic patients.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Diabetes Research

Background:

  • Type 2 diabetes (T2D) is linked to cardiovascular complications.
  • Large conductance calcium-activated potassium (BK) channels regulate vascular tone.
  • The role of BK channels in diabetic coronary microvascular dysfunction is not well understood.

Purpose of the Study:

  • To investigate BK channel function, expression, and vasodilation in coronary arterioles from T2D patients.
  • To determine if BK channel abnormalities contribute to coronary microvascular dysfunction in T2D.

Main Methods:

  • Isolated coronary arterioles and smooth muscle cells from T2D and non-diabetic patients.
  • Electrophysiological recordings of single BK channel currents.
  • Immunoblot analysis for BK channel subunit expression.
  • Functional assessment of BK channel-mediated vasodilation.

Main Results:

  • BK channel sensitivity to calcium and voltage was reduced in T2D patients.
  • BK channel open probability was significantly decreased in diabetic coronary arterioles.
  • BK channel-mediated vasodilation and activation were impaired in T2D.
  • Protein expression of BK-α and BK-β1 subunits was downregulated in T2D.

Conclusions:

  • BK channel function and vasodilation are abnormal in the coronary microvasculature of T2D patients.
  • Decreased BK channel expression and altered intrinsic properties contribute to this dysfunction.
  • These findings highlight a potential mechanism for coronary microvascular dysfunction in type 2 diabetes.

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