Potassium currents in ventricular myocytes from genetically diabetic rats

Area of Science:

• Cardiovascular Physiology
• Diabetology
• Electrophysiology

Background:

• Previous studies showed longer action potential duration in diabetic rat ventricular myocytes without altered calcium channel density.
• WBN/Kob rats model non-insulin-dependent diabetes mellitus, developing hyperglycemia with age.

Purpose of the Study:

• To investigate alterations in potassium currents, specifically transient outward current (I(to)), in ventricular myocytes of genetically diabetic WBN/Kob rats.
• To determine the contribution of I(to) to the prolonged action potential duration observed in diabetic rat hearts.

Main Methods:

• Electrophysiological recordings of potassium currents in ventricular myocytes from diabetic and age-matched control WBN/Kob rats.
• Comparison of I(to) density, inactivation curves, and recovery from inactivation between groups.
• Assessment of aging effects on I(to) in both diabetic and control rats.

Main Results:

• Ventricular myocytes from 17- to 19-month-old diabetic rats showed significantly reduced transient outward current (I(to)) density compared to age-matched controls.
• I(to) density decreased with age in both diabetic and control rats, but the decline was accelerated in diabetic rats.
• No significant alterations were found in steady-state inactivation curves or recovery from inactivation of I(to), nor in other outward currents.

Conclusions:

• The prolonged action potential duration in ventricular myocytes of genetically diabetic WBN/Kob rats is primarily caused by a depressed transient outward potassium current (I(to)).
• The diabetic state accelerates age-related decline in I(to) density, contributing to cardiac electrophysiological abnormalities.