Sarcoplasmic reticulum calcium load regulates rat arterial smooth muscle calcium sparks and transient K Ca currents

The regulation of calcium (Ca 2+ ) sparks and transient calcium‐sensitive K + (K Ca ) currents by acute changes in sarcoplasmic reticulum (SR) Ca 2+ load ([Ca 2+ ] SR ) was investigated in rat cerebral artery smooth muscle cells using laser‐scanning confocal microscopy in combination with patch clamp electrophysiology. [Ca 2+ ] SR was elevated by: (i) increasing the activity of the SR Ca 2+ ‐ATPase with an anti‐phospholamban monoclonal antibody, or (ii) blocking Ca 2+ release from the SR with tetracaine, a membrane‐permeant, reversible ryanodine‐sensitive Ca 2+ release (RyR) channel blocker. Alternatively, [Ca 2+ ] SR was progressively decreased over time with a low concentration of thapsigargin (20 n m ), a SR Ca 2+ ‐ATPase blocker. An elevation in [Ca 2+ ] SR increased Ca 2+ spark and transient K Ca current frequency, but did not alter the amplitude, decay or spatial spread of Ca 2+ sparks or the coupling ratio or amplitude correlation between Ca 2+ sparks and evoked transient K Ca currents. Decreasing [Ca 2+ ] SR reduced Ca 2+ spark frequency, amplitude and spatial spread and this reduced transient K Ca current frequency and amplitude. However, even when mean Ca 2+ spark amplitude and spread decreased by up to 47 and 56 % of control, respectively, the coupling ratio or amplitude correlation between Ca 2+ sparks and transient K Ca currents was not affected. These data demonstrate that acute changes in [Ca 2+ ] SR regulate Ca 2+ sparks and transient K Ca currents in arterial smooth muscle cells.