Key Points
- To determine how reducing extracellular calcium influx affects voltage-dependent and calcium-activated potassium currents in vascular smooth muscle cells isolated from rat small mesenteric arteries.
- Measured potassium currents using whole-cell patch-clamp electrophysiology from holding potentials of -20 mV and -60 mV in rat mesenteric artery myocytes.
- Reduced calcium influx by adding external cadmium (Cd2+) or lowering external calcium concentration to 0.2 mM.
- Assessed pharmacological modulation using the calcium chelator BAPTA (10 mM), calcium channel blocker cadmium, calcium-activated potassium channel inhibitor iberiotoxin (100 nM), and L-type calcium channel agonist BAY K 8644 (1 µM).
- Decreasing calcium influx reduced calcium-activated potassium currents measured at a holding potential of -20 mV at voltages >0 mV.
- Decreasing calcium influx increased potassium currents measured from a holding potential of -60 mV at -30 to +20 mV, yielding peak difference currents of 75 ± 13 pA with Cd2+ (n = 8) and 120 ± 20 pA with low Ca2+ (n = 9) at 0 mV.
- In the presence of iberiotoxin, Cd2+ increased voltage-dependent potassium currents at all potentials positive to -30 mV, whereas BAY K 8644 decreased them.
Structured PICO
PPopulationMyocytes from rat small mesenteric arteries
IInterventionReducing Ca2+ influx by adding external Cd2+ or lowering external Ca2+ to 0.2 mM
CComparatorControl conditions
OOutcomeChanges in K+ currents (I(K)) measured from holding potentials of -20 mV and -60 mVsurrogate
Ca2+ influx increases Ca2+-activated K+ channels and decreases voltage-dependent K+ currents in rat mesenteric arterial myocytes, which could contribute to membrane depolarization and force maintenance.