Key result
Experimentally induced type 1 diabetes in rats significantly increased action potential duration and reduced firing rate, upstroke velocity, and rate of diastolic depolarization in AVN myocytes.
Why the study?
Does experimentally induced type 1 diabetes alter atrioventricular nodal electrophysiology at the cellular level in rats?
Does experimentally induced type 1 diabetes alter atrioventricular nodal electrophysiology at the cellular level in rats?
Experimentally induced type 1 diabetes leads to significant remodeling of atrioventricular nodal cellular electrophysiology in a rat model.
No immediate clinical implications; leaves open whether type 1 diabetes remodels human AV nodal electrophysiology.
The present study was conducted to evaluate whether experimentally induced type 1 diabetes results in alterations to atrioventricular nodal (AVN) electrophysiology at the cellular level. Spontaneous action potentials (APs) and ionic currents were recorded from AVN myocytes isolated from the hearts of control rats and from those with streptozotocin-induced diabetes. Perforated patch-clamp recordings were used to assess changes in cellular AP parameters and in ionic currents. Type 1 diabetes significantly increased AP duration, whilst reducing AP firing rate, upstroke velocity and rate of diastolic depolarization. The diabetes-induced changes in AP parameters were accompanied by a significant leftward shift in the zero current potential under voltage clamp, a reduction in peak L-type Ca(2+) current density and reduced amplitude of delayed rectifier and hyperpolarization-activated currents. These findings demonstrate that experimentally induced type 1 diabetes can lead to remodelling of AVN cellular electrophysiology.
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Yuill et al. (2009) studied Type 1 diabetes. Streptozotocin-induced type 1 diabetes vs. Control rats was evaluated on Atrioventricular nodal (AVN) electrophysiology (action potential parameters and ionic currents). Experimentally induced type 1 diabetes in rats significantly increased action potential duration and reduced firing rate, upstroke velocity, and rate of diastolic depolarization in AVN myocytes.
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