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Related Experiment Videos

Cyclosporin A potentiates receptor-activated [Ca2+]c increase

A Lo Russo1, A C Passaquin, C Cox

  • 1Pharmacology Group, School of Pharmacy University of Lausanne, Switzerland.

Journal of Receptor and Signal Transduction Research
|January 1, 1997
PubMed
Summary

Cyclosporin A (CsA) potentiates vasoconstriction by increasing intracellular calcium. This effect occurs upstream of G protein activation, suggesting CsA targets receptors, impacting smooth muscle cell function.

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Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Cell Biology

Background:

  • Immunosuppressant cyclosporin A (CsA) is linked to hypertension.
  • This hypertension is thought to stem from drug-induced vasoconstriction.

Purpose of the Study:

  • To investigate the mechanism by which CsA affects cytosolic calcium concentration ([Ca2+]c) in rat aortic smooth muscle cells.
  • To determine if CsA's effect on [Ca2+]c is related to G protein activation or occurs at an earlier signaling step.

Main Methods:

  • Fura-2 and 45Ca2+ efflux assays were used to measure [Ca2+]c.
  • Rat aortic smooth muscle cells were preincubated with CsA and stimulated with various agonists (vasopressin, serotonin, endothelin-1, angiotensin II).
  • Inositol phosphate (InsPn) formation and G protein activation (using aluminium tetrafluoride) were also assessed.

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Main Results:

  • CsA preincubation potentiated agonist-induced increases in [Ca2+]c and InsPn formation.
  • These CsA effects were independent of cyclophilin or calcineurin inhibition.
  • CsA did not potentiate [Ca2+]c or InsPn increases induced by direct G protein stimulation.

Conclusions:

  • CsA potentiates vasoconstriction by enhancing agonist-induced calcium influx in smooth muscle cells.
  • The mechanism involves potentiation of InsPn formation upstream of G protein activation, likely at the receptor level.
  • This CsA action contributes to the hypertension associated with its use.