Key Points
- To determine the pharmacological effects of gadolinium on the delayed rectifier potassium current and electrical repolarization in isolated ventricular myocytes.
- Recorded membrane currents in isolated guinea-pig ventricular myocytes using whole-cell patch-clamp electrophysiology.
- Stretched single myocytes using carbon fibers to assess stretch-activated resting calcium alterations.
- Modeled repolarization dynamics and calcium handling using the OXSOFT HEART computational simulation program.
- Gadolinium blocked 70% of the delayed rectifier potassium tail current at 100 µM, with a half-maximal effective concentration (EC50) of 24 µM.
- Action potential duration shortened with gadolinium alone but lengthened following L-type calcium channel inhibition with 5 µM nifedipine.
- Application of 10 µM gadolinium failed to suppress stretch-induced elevations in resting calcium, reflecting combined inhibition of potassium repolarizing currents and sodium-calcium exchange.
Structured PICO
PPopulationIsolated guinea-pig ventricular myocytes
IInterventionGadolinium (Gd3+)
OOutcomeDelayed rectifier potassium current (IK) and action potential durationsurrogate
When using Gadolinium as a blocker of stretch-activated channels, its off-target blockade of delayed rectifier potassium current and L-type calcium current must be considered.