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Effects of loop diuretics on angiotensin II-stimulated vascular smooth muscle cell growth

P Muñiz1, A Fortuño, G Zalba

  • 1Division of Cardiovascular Pathophysiology, School of Medicine, University of Navarra, Pamplona, Spain.

Abstract

Insights

Torasemide inhibits angiotensin II-induced protein synthesis in rat vascular smooth muscle cells, unlike furosemide. This effect is not mediated by the Na(+), K(+), 2Cl(-) co-transporter, suggesting a novel mechanism for torasemide.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Nephrology

Background:

  • Torasemide and furosemide are diuretics targeting the Na(+), K(+), 2Cl(-) co-transporter in the loop of Henle.
  • Angiotensin II (Ang II) is implicated in vascular smooth muscle cell (VSMC) growth.

Purpose of the Study:

  • To investigate the effects of torasemide and furosemide on Ang II-induced VSMC growth in spontaneously hypertensive rats (SHR).

Main Methods:

  • Cultured aortic VSMCs from SHR were used.
  • Cell growth assessed via [3H]thymidine and [3H]leucine incorporation (DNA and protein synthesis).
  • Cell proliferation measured using a colorimetric assay.

Main Results:

  • Ang II significantly increased DNA synthesis, protein synthesis, and proliferation in VSMCs.
  • Torasemide dose-dependently reduced Ang II-induced protein synthesis (IC50: 7.7±0.8x10⁻⁷ M).
  • Furosemide did not affect Ang II-induced protein synthesis, DNA synthesis, or proliferation.

Conclusions:

  • Torasemide, but not furosemide, inhibits Ang II-induced protein synthesis in SHR VSMCs.
  • This inhibitory action of torasemide is independent of the Na(+), K(+), 2Cl(-) co-transport mechanism.

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