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Developmental changes in the delayed rectifier K+ channels in mouse heart
Circulation Research
|July 1, 1996
Summary
Cardiac delayed rectifier K+ current (IK) expression changes significantly during mouse heart development. Researchers found that IK channels, including IKr and IKs, are present in fetal and neonatal stages but absent in adult mouse hearts.
Area of Science:
- Cardiovascular Physiology
- Ion Channel Biology
- Developmental Biology
Background:
- Cardiac ion channel function, including transient outward and inwardly rectifying K+ currents, is known to be age-dependent.
- Limited information exists regarding age-related alterations in the cardiac delayed rectifier K+ current (IK), comprising rapidly (IKr) and slowly (IKs) activating components.
Purpose of the Study:
- To investigate developmental changes in cardiac delayed rectifier K+ (IK) channels within fetal, neonatal, and adult mouse ventricles.
Main Methods:
- Utilized conventional microelectrodes to measure action potential duration.
- Employed voltage clamp techniques to record macroscopic IK currents.
- Conducted radioligand assays to quantify [3H]dofetilide binding sites.
Main Results:
- Action potential duration prolongation by the IKr blocker dofetilide significantly decreased from fetal to neonatal stages and was absent in adults.
- IKr was the sole IK component in fetal ventricular myocytes, with both IKr and IKs present in neonates.
- IKs became dominant in later neonatal stages, and neither IKr nor IKs was detected in adult ventricular myocytes; [3H]dofetilide binding sites were also absent in adults.
Conclusions:
- Cardiac delayed rectifier K+ (IK) channel expression is developmentally regulated in the mouse heart.
- These findings highlight significant shifts in IK channel composition and function from fetal to adult life.