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Elementary calcium signaling in arterial smooth muscle

Authors

  • G. Fan
  • Y. Cui
  • M. Gollasch
  • M. Kassmann

Journal

  • Channels

Citation

  • Channels 13 (1): 505-519

Abstract

  • Vascular smooth muscle cells (VSMCs) of small peripheral arteries contribute to blood pressure control by adapting their contractile state. These adaptations depend on the VSMC cytosolic Ca(2+) concentration, regulated by complex local elementary Ca(2+) signaling pathways. Ca(2+) sparks represent local, transient, rapid calcium release events from a cluster of ryanodine receptors (RyRs) in the sarcoplasmic reticulum. In arterial SMCs, Ca(2+) sparks activate nearby calcium-dependent potassium channels, cause membrane hyperpolarization and thus decrease the global intracellular [Ca(2+)] to oppose vasoconstriction. Arterial SMC Ca(V)1.2 L-type channels regulate intracellular calcium stores content, which in turn modulates calcium efflux through RyRs. Ca(V)3.2 T-type channels contribute to a minor extend to Ca(2+) spark generation in certain types of arteries. Their localization within cell membrane caveolae is essential. We summarize present data on local elementary calcium signaling (Ca(2+) sparks) in arterial SMCs with focus on RyR isoforms, large-conductance calcium-dependent potassium (BK(Ca)) channels, and cell membrane-bound calcium channels (Ca(V)1.2 and Ca(V)3.2), particularly in caveolar microdomains.


DOI

doi:10.1080/19336950.2019.1688910