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A Ca²⁺-permeable non-selective cation channel activated by depletion of internal Ca²⁺ stores in single rabbit portal vein myocytes

A. P. Albert and W. A. Large

In vascular smooth muscle cells many agonists cause the release of Ca²⁺ ions from internal stores. An important problem concerns the mechanism by which the intracellular stores are refilled subsequent to depletion. In the present study, we describe the properties of a Ca²⁺-permeable non-selective cation channel current that is activated in rabbit portal vein myocytes by depletion of internal Ca²⁺ stores. Application of cyclopiazonic acid (CPA), which depletes internal Ca²⁺ stores, activated whole-cell currents that had a reversal potential (E_r) of about +50 mV in 1.5 mM external Ca²⁺ (Ca). In 0 mM Ca, the currents were larger and E_r was ~0 mV. Application of CPA and caffeine during cell-attached recording activated single inward channel currents at negative potentials, which had a slope conductance of 2-3 pS and an E_r of +20 mV. The slope conductance in 0 and 110 mM Ca was 7 and 1.5 pS, respectively, and E_r values indicated that these non-selective cation channels are highly permeable to Ca²⁺ ions. Bath application of the cell-permeant Ca²⁺ chelator, BAPTA-AM, also activated similar currents, indicating that these channels are not activated by Ca²⁺. Spontaneous channel currents with similar properties to store-operated channels were observed in some patches. Application of W-7, an inhibitor of the Ca²⁺-binding protein calmodulin, also activated similar Ca²⁺-permeable channel currents. In conclusion, it is demonstrated that agents that deplete Ca²⁺ stores and inhibit calmodulin binding activate Ca²⁺-permeable non-selective cation channel currents in rabbit portal vein myocytes. These channels may have an important role in vascular smooth muscle in providing an influx of Ca²⁺ to refill depleted internal Ca²⁺ stores and appear to possess different characteristics to store-operated channels described in other vascular smooth muscle preparations.

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