Increased transient receptor potential channel TRPC3 expression in spontaneously hypertensive rats
Daoyan Liu1, Alexandra Scholze, Zhiming Zhu
1Medizinische Klinik IV, Charité Campus Benjamin Franklin, Berlin, Germany.
American Journal of Hypertension
|November 11, 2005
Summary
Primary hypertension is linked to altered calcium regulation. This study found increased transient receptor potential canonical channel 3 (TRPC3) expression and calcium influx in hypertensive rats, suggesting TRPC3’s role in hypertension.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Physiology
Background:
- Cytosolic calcium dysregulation is implicated in primary hypertension.
- The specific role of calcium-permeable transient receptor potential canonical channel 3 (TRPC3) in primary hypertension remains unevaluated.
Purpose of the Study:
- To investigate the expression and function of TRPC3 in the context of primary hypertension.
- To determine if TRPC3 contributes to altered calcium homeostasis in spontaneously hypertensive rats (SHR).
Main Methods:
- TRPC3 expression was quantified using in-cell Western assays.
- Small interfering RNA (siRNA) was employed for gene silencing (knockdown) of TRPC3.
- Cytosolic calcium levels were measured using fura-2 fluorescence.
Main Results:
- TRPC3 expression was significantly elevated in monocytes from SHR compared to normotensive Wistar-Kyoto rats (WKY).
- Calcium influx across the plasma membrane and thapsigargin-induced calcium increase were higher in SHR.
- These differences were abolished by the TRP channel blocker SKF-96365.
- TRPC3 knockdown in SHR monocytes reduced TRPC3 expression, calcium influx, and sustained calcium levels.
Conclusions:
- This study provides the first evidence of increased TRPC3 channel expression in SHR.
- Elevated TRPC3 expression correlates with increased TRPC3-mediated calcium influx in primary hypertension.
