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Related Experiment Videos

Tolerance for ATP-insensitive K(ATP) channels in transgenic mice.

J C Koster1, A Knopp, T P Flagg

  • 1Department of Cell Biology, Washington University School of Medicine, St Louis, MO, USA.

Circulation Research
|November 22, 2001
PubMed
Summary

Altered cardiac ATP-sensitive potassium (KATP) channels in mice showed reduced ATP sensitivity but maintained normal heart function. This suggests cardiac KATP channels tolerate reduced ATP sensitivity, unlike those in pancreatic beta-cells.

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Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Ion Channel Biology

Background:

  • Sarcolemmal ATP-sensitive potassium (KATP) channels play a crucial role in cardiac function.
  • Understanding their regulation and sensitivity to ATP is vital for cardiac health.

Purpose of the Study:

  • To investigate the functional consequences of reduced ATP sensitivity in cardiac KATP channels.
  • To compare the effects of altered KATP channel function in the heart versus pancreatic beta-cells.

Main Methods:

  • Generation of transgenic mice expressing GFP-tagged Kir6.2 subunits with reduced ATP sensitivity under the cardiac alpha-myosin heavy chain promoter.
  • Electrocardiography in conscious animals.
  • Excised membrane patch-clamp and whole-cell voltage-clamp electrophysiology on isolated myocytes.

Related Experiment Videos

  • Assessment of KATP channel density and conductance.

    • Main Results:

    • Transgenic mice exhibited normal fertility and overall health, with a modest decrease in mean heart rate.
    • Cardiac KATP channels in transgenic mice showed significantly reduced sensitivity to ATP inhibition (K(1/2) = 2.7 mmol/L vs. 51 micromol/L in controls).
    • Counterintuitively, KATP channel density was reduced ~4-fold, leading to lower overall KATP conductance, with no observed action potential shortening.

    Conclusions:

    • Cardiac KATP channels demonstrate a remarkable tolerance for reduced ATP sensitivity.
    • Altered cardiac KATP channel function does not impair cardiac electrical activity under basal conditions.
    • This highlights differential roles and regulatory mechanisms of KATP channels in cardiac myocytes versus pancreatic beta-cells.