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Transient receptor potential canonical type 3 channels and blood pressure in humans

Florian Thilo1, Daniel Baumunk, Hans Krause

  • 1Medizinsche Klinik Nephrologie, Institut für Pathologie, Charité Campus Benjamin Franklin, Berlin, Germany.

Journal of Hypertension
|May 7, 2009
PubMed

Insights

Transient receptor potential canonical type 3 (TRPC3) channels are linked to blood pressure regulation. Higher TRPC3 expression in human kidney tissue correlates with elevated systolic blood pressure, suggesting a role in hypertension.

Area of Science:

  • Cardiovascular Physiology
  • Renal Physiology
  • Molecular Biology

Background:

  • Transient receptor potential canonical type 3 (TRPC3) cation channels are implicated in blood pressure regulation.
  • Previous studies have not investigated TRPC3 expression in human renal tissue.

Purpose of the Study:

  • To test the hypothesis that TRPC3 expression in human renal tissue is associated with blood pressure in patients.
  • To investigate the role of TRPC3 in human renal vascular endothelium.

Main Methods:

  • TRPC3 expression was analyzed in cultured human endothelial cells and human renal tissue using immunoblotting, immunohistochemistry, and quantitative real-time reverse transcriptase-PCR.
  • Vascular endothelial growth factor (VEGF) isoform 121 was administered to cultured cells to assess its effect on TRPC3 and VEGF receptor type 2 (VEGFR2) expression.
  • Calcium influx was measured and modulated using specific inhibitors.

Main Results:

  • VEGF 121 significantly reduced TRPC3 and VEGFR2 expression in endothelial cells, an effect partially mediated by phosphatidylinositol 3-kinase signaling.
  • Downregulation of TRPC3 expression correlated with reduced calcium influx, confirming functional importance.
  • TRPC3 expression was significantly higher in patients with systolic blood pressure (SBP) > 140 mmHg compared to those with SBP ≤ 140 mmHg (P < 0.01).

Conclusions:

  • TRPC3 expression in human renal tissue, including vascular endothelium, is associated with blood pressure regulation.
  • These findings support a role for TRPC3 in the pathophysiology of human hypertension.
Abstract

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