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Updated: May 16, 2026

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Published on: March 12, 2013

Alterations in ventricular K(ATP) channel properties during aging.

Li Bao¹, Eylem Taskin, Monique Foster

¹Pediatrics, NYU School of Medicine, New York, NY 10016, USA.

|November 24, 2012

Summary

This summary is machine-generated.

Aging compromises the protective function of ATP-sensitive potassium (K(ATP)) channels in the heart. This diminished channel activity in aged hearts reduces protection against ischemic injury, increasing cardiovascular risk.

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Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles

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Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles

Ex Vivo Assessment of Contractility, Fatigability and Alternans in Isolated Skeletal Muscles

Published on: November 1, 2012

Area of Science:

Cardiovascular Physiology
Aging Research
Ion Channel Biology

Background:

Coronary heart disease is a leading cause of mortality, with aging reducing cardiovascular resilience to ischemic injury.
ATP-sensitive potassium (K(ATP)) channels are known cardioprotective mechanisms against myocardial ischemia.
Understanding age-related changes in K(ATP) channel function is crucial for mitigating ischemic damage in older individuals.

Purpose of the Study:

To investigate the impact of aging on cardiac K(ATP) channel function and expression.
To determine the mechanisms underlying age-associated alterations in K(ATP) channel activity.
To model the functional consequences of these changes on cardiac action potentials during metabolic stress.

Main Methods:

Comparison of K(ATP) channel subunit mRNA and protein levels in young (4-month-old) and aged (26-month-old) Fischer 344 rats.
Electrophysiological recordings (whole-cell and inside-out patch-clamp) of K(ATP) channel currents in ventricular myocytes.
Development of an empirical model to simulate K(ATP) channel activity and action potential changes under varying cytosolic ATP levels.

Main Results:

Cardiac K(ATP) channel subunit expression (mRNA and protein) remained unchanged with aging.
Whole-cell K(ATP) current density was significantly reduced in aged rat and mouse ventricular myocytes.
While unitary conductance was unaltered, aged K(ATP) channels exhibited enhanced inhibition by cytosolic ATP, leading to diminished channel activity.

Conclusions:

Aging impairs cardiac K(ATP) channel function primarily through post-transcriptional mechanisms, specifically increased ATP sensitivity.
The reduced K(ATP) channel activity in aged hearts diminishes their protective capacity against ischemic events.
These findings highlight a critical age-related vulnerability in myocardial protection, necessitating further research into therapeutic interventions.