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The regulation of calcium (Ca2+) sparks and transient calcium-sensitive K+ (KCa) currents by acute changes in sarcoplasmic reticulum (SR) Ca2+ load ([Ca2+]SR) was investigated in rat cerebral artery smooth muscle cells using laser-scanning confocal microscopy in combination with patch clamp electrophysiology. [Ca2+]SR was elevated by: (i) increasing the activity of the SR Ca2+-ATPase with an anti-phospholamban monoclonal antibody, or (ii) blocking Ca2+ release from the SR with tetracaine, a membrane-permeant, reversible ryanodine-sensitive Ca2+ release (RyR) channel blocker. Alternatively, [Ca2+]SR was progressively decreased over time with a low concentration of thapsigargin (20 nM), a SR Ca2+-ATPase blocker. An elevation in [Ca2+]SR increased Ca2+ spark and transient KCa current frequency, but did not alter the amplitude, decay or spatial spread of Ca2+ sparks or the coupling ratio or amplitude correlation between Ca2+ sparks and evoked transient KCa currents. Decreasing [Ca2+]SR reduced Ca2+ spark frequency, amplitude and spatial spread and this reduced transient KCa current frequency and amplitude. However, even when mean Ca2+ spark amplitude and spread decreased by up to 47 and 56 % of control, respectively, the coupling ratio or amplitude correlation between Ca2+ sparks and transient KCa currents was not affected. These data demonstrate that acute changes in [Ca2+]SR regulate Ca2+ sparks and transient KCa currents in arterial smooth muscle cells.
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