Am J Physiol Cell Physiol AJP: Gastrointestinal and Liver Physiology
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Am J Physiol Cell Physiol 280: C481-C490, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 3, C481-C490, March 2001

Voltage dependence of the coupling of Ca2+ sparks to BKCa channels in urinary bladder smooth muscle

Gerald M. Herrera1, Thomas J. Heppner2, and Mark T. Nelson1,2

Departments of 1 Molecular Physiology and Biophysics and 2 Pharmacology, University of Vermont College of Medicine, Burlington, Vermont 05405

Large-conductance Ca2+-dependent K+ (BKCa) channels play a critical role in regulating urinary bladder smooth muscle (UBSM) excitability and contractility. Measurements of BKCa currents and intracellular Ca2+ revealed that BKCa currents are activated by Ca2+ release events (Ca2+ sparks) from ryanodine receptors (RyRs) in the sarcoplasmic reticulum. The goals of this project were to characterize Ca2+ sparks and BKCa currents and to determine the voltage dependence of the coupling of RyRs (Ca2+ sparks) to BKCa channels in UBSM. Ca2+ sparks in UBSM had properties similar to those described in arterial smooth muscle. Most Ca2+ sparks caused BKCa currents at all voltages tested, consistent with the BKCa channels sensing ~10 µM Ca2+. Membrane potential depolarization from -50 to -20 mV increased Ca2+ spark and BKCa current frequency threefold. However, membrane depolarization over this range had a differential effect on spark and current amplitude, with Ca2+ spark amplitude increasing by only 30% and BKCa current amplitude increasing 16-fold. A major component of the amplitude modulation of spark-activated BKCa current was quantitatively explained by the known voltage dependence of the Ca2+ sensitivity of BKCa channels. We, therefore, propose that membrane potential, or any other agent that modulates the Ca2+ sensitivity of BKCa channels, profoundly alters the coupling strength of Ca2+ sparks to BKCa channels.

guinea pig; sarcoplasmic reticulum; ryanodine receptor; iberiotoxin; thapsigargin; large-conductance Ca2+-activated K+ channels


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