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Temporal changes in atrial EC-coupling during prolonged stimulation with endothelin-1.

Martin D Bootman1, Dagmar Harzheim, Ioannis Smyrnias

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Endothelin-1 (ET-1) causes complex calcium signaling changes in atrial cells, leading to varied inotropic effects and pro-arrhythmic events. These effects involve inositol trisphosphate receptors (InsP3Rs), impacting cardiac function.

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Area of Science:

  • Cardiovascular Physiology
  • Cellular Electrophysiology
  • Molecular Cardiology

Background:

  • Endothelin-1 (ET-1) is a potent vasoconstrictor and signaling molecule with known cardiac effects.
  • G(q)-coupled receptor activation by ET-1 influences intracellular calcium (Ca2+) dynamics.
  • Atrial myocytes exhibit complex responses to prolonged stimulation, impacting contractility and rhythm.

Purpose of the Study:

  • To characterize the effects of prolonged Endothelin-1 (ET-1) stimulation on Ca2+ signaling in atrial myocytes.
  • To investigate the mechanisms underlying ET-1-induced inotropic changes and pro-arrhythmic events.
  • To determine the role of inositol trisphosphate receptors (InsP3Rs) in mediating ET-1's actions.

Main Methods:

  • Acutely isolated atrial myocytes were subjected to prolonged ET-1 stimulation.
  • Calcium (Ca2+) signaling, including sparks, waves, and transients, was monitored.
  • Pharmacological agents, including InsP3R antagonists, were used to probe signaling pathways.

Main Results:

  • ET-1 induced a complex sequence of negative and positive inotropy.
  • Pro-arrhythmic spontaneous Ca2+ transients (SCTs) of varying spatial and temporal complexity were observed.
  • Stimulation of InsP3Rs mimicked ET-1's positive inotropic effects and SCT generation.
  • InsP3R antagonism reduced ET-1-induced SCTs and partially attenuated positive inotropy.

Conclusions:

  • ET-1 triggers diverse Ca2+ signaling responses in atrial myocytes through multiple pathways.
  • InsP3R activation is a significant mechanism contributing to ET-1's positive inotropic effects and pro-arrhythmic potential.
  • Understanding these complex signaling events is crucial for comprehending ET-1's role in cardiac physiology and pathology.