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Articles in PresS, published online ahead of print September 21, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00326.2001
Submitted on July 27, 2001
Accepted on September 12, 2001
1 Physiology, University of Extremadura, Caceres, Spain
2 Pharmacology, University of Vermont, Burlington, VT, USA
3 Anatomy and Neurobiology, University of Vermont, Burlington, VT, USA; Pharmacology, University of Vermont, Burlington, VT, USA
* To whom correspondence should be addressed. E-mail: gmawe{at}zoo.uvm.edu.
We sought to elucidate the regulation of gallbladder smooth muscle (GBSM) excitability by localized Ca2+ release events (sparks) and large-conductance Ca2+-dependent (BK) channels by determining whether sparks exist in GBSM, and if so, whether they activate BK channels. Sparks were identified in isolated GBSM loaded with fluo-4. Each spark was associated with a transient outward current, suggesting communication of ryanodine receptor-channels (RyRs) with BK channels. This was confirmed by the inhibition of outward currents with iberiotoxin (100 nM), thapsigargin (200 nM), and ryanodine (10 µM). In current clamp mode, the transient BK currents were associated with brief membrane hyperpolarizations (10.9 ± 1.3 mV). As transient BK currents could dampen GBSM excitability, we tested whether CCK attenuates these events. CCK (10 nM) reduced the amplitude and frequency of transient BK currents, and subsequent caffeine application restored transient BK current activity. These results support the concept that RyRs and BK channels play contribute to the regulation of GBSM excitability, and that CCK can act in part by inhibiting this pathway.
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