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Related Experiment Videos

Extracellular ATP regulates glomerular endothelial cell function

H Pavenstädt1, A Henger, V Briner

  • 1Department of Nephrology, Albert-Ludwigs-Universität, Freiburg, Germany.

Journal of Autonomic Pharmacology
|December 1, 1996
PubMed
Summary
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Extracellular adenosine triphosphate (ATP) influences glomerular endothelial cell (GEC) function by altering membrane voltage and intracellular calcium. These effects are mediated by the P2y2 receptor, impacting kidney filtration barrier processes.

Area of Science:

  • Cell biology
  • Renal physiology
  • Molecular pharmacology

Background:

  • Glomerular endothelial cells (GECs) are crucial components of the renal filtration barrier.
  • GECs play a role in glomerular pathophysiological processes.
  • Recent advancements have enabled the culture of GECs, facilitating experimental investigation.

Purpose of the Study:

  • To investigate the effects of extracellular adenosine triphosphate (ATP) on GEC membrane potential and intracellular calcium activity.
  • To elucidate the purinergic receptor subtypes involved in ATP signaling in GECs.

Main Methods:

  • Patch clamp technique in the fast whole-cell configuration was used to measure membrane voltage.
  • Fura-2 imaging was employed to quantify intracellular calcium activity ([Ca2+]i) in single GECs.

Related Experiment Videos

  • Various purine nucleotides were tested to determine their potency in stimulating [Ca2+]i and inositol phosphate formation.
  • Main Results:

    • GECs exhibit a stable resting membrane potential of -88 mV.
    • ATP induced a transient hyperpolarization followed by a sustained depolarization, inhibited by flufenamate.
    • ATP stimulated a biphasic increase in [Ca2+]i, with an extracellular calcium-dependent plateau phase.

    Conclusions:

    • Extracellular ATP modulates membrane voltage and intracellular calcium levels in cultured GECs.
    • The P2y2 receptor is identified as the primary mediator of ATP's effects on GEC membrane voltage and [Ca2+]i.
    • These findings contribute to understanding the role of purinergic signaling in glomerular endothelial cell function.