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Exploring Arterial Smooth Muscle Kv7 Potassium Channel Function using Patch Clamp Electrophysiology and Pressure Myography
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Overexcited MaxiK and KATP channels underlie obstructive jaundice-induced vasoconstrictor hyporeactivity of arterial

Ya-Wei Yuan1, Long Wang2, Zhan-Ying Lu3

  • 1Department of Anesthesiology, Renji Hospital affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.

Scientific Reports
|December 22, 2016
PubMed

Insights

Obstructive jaundice causes vascular hyporesponsiveness by altering MaxiK and KATP channels. Bile duct ligation in rats promoted these channel currents, contributing to vascular dysfunction.

Area of Science:

  • Physiology
  • Vascular Biology
  • Channelopathies

Background:

  • Obstructive jaundice is known to induce vascular hyporesponsiveness.
  • The underlying molecular mechanisms, particularly ion channel involvement, remain incompletely understood.

Purpose of the Study:

  • To investigate the roles of MaxiK (BK) channels and ATP-sensitive potassium (KATP) channels in cholestasis-induced vascular dysfunction.
  • To explore the impact of bile duct ligation (BDL) on vascular reactivity and ion channel function in rat thoracic aorta.

Main Methods:

  • Isolated thoracic aorta from sham-operated and BDL rats were used to assess norepinephrine (NE)-induced contraction.
  • Whole-cell patch clamp recordings were performed on isolated aortic smooth muscle cells to investigate MaxiK and KATP channel function.
  • The expression levels of MaxiK and KATP channel subunits were analyzed.

Main Results:

  • NE-induced vascular contraction was significantly blunted in BDL rats compared to sham controls.
  • Administration of charybdotoxin (MaxiK channel blocker) and glibenclamide (KATP channel blocker) partially restored vascular responsiveness in BDL rats.
  • BDL significantly increased MaxiK and KATP channel currents in aortic smooth muscle cells, with a notable upregulation of auxiliary subunits (MaxiK-β1, SUR2B).

Conclusions:

  • MaxiK and KATP channels are critically involved in the vascular hyporesponsiveness observed in rats with obstructive jaundice.
  • The functional upregulation of these channels, particularly their auxiliary subunits, contributes to cholestasis-induced vascular dysfunction.

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