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Updated: Dec 10, 2025
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Published on: September 17, 2015
TRPC6 participates in the development of blood pressure variability increase in sino-aortic denervated rats
Yu Wang1, Ling Liu2, Hongmei Tao1
1Department of Cardiovascular Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Insights
Increased blood pressure variability (BPV) is linked to cardiovascular issues. This study shows that the TRPC6 channel, not TRPC3, plays a key role in raising BPV in rats after sino-aortic denervation.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Hypertension Research
Background:
- Elevated blood pressure variability (BPV) is a significant predictor of cardiovascular morbidity and mortality.
- Understanding the mechanisms driving BPV is crucial for developing targeted interventions.
- The cation channel transient receptor potential canonical 6 (TRPC6) has been implicated in various cardiovascular diseases.
Purpose of the Study:
- To investigate the role of TRPC6 in the development of increased BPV.
- To determine if TRPC6 expression is altered in a rat model of elevated BPV.
- To assess the functional impact of TRPC6 modulation on BPV.
Main Methods:
- A rat model of increased BPV was established using sino-aortic denervation (SAD).
- Hemodynamic parameters, including BPV, were measured non-invasively.
- TRPC6 and TRPC3 expression levels in myocardial and thoracic aortic tissues were quantified using Western Blot, immunofluorescence, and qRT-PCR.
- The effects of TRPC6 activation and inhibition on BPV were evaluated in SAD rats.
Main Results:
- SAD rats exhibited significantly increased systolic and diastolic BPV without changes in mean blood pressure or heart rate.
- Both mRNA and protein levels of TRPC6 were substantially elevated in the myocardium and thoracic aorta of SAD rats.
- TRPC3 expression showed no significant changes.
- Activation of TRPC6 exacerbated BPV, while inhibition attenuated it in a dose-dependent manner.
Conclusions:
- TRPC6 expression is significantly upregulated in the myocardium and thoracic aorta following SAD.
- TRPC6, but not TRPC3, appears to play a critical role in the development and maintenance of elevated BPV.
- Targeting TRPC6 may offer a therapeutic strategy for managing BPV and associated cardiovascular risks.
Abstract:
Increased blood pressure variability (BPV) has been proved to be associated with cardiovascular morbidity and mortality. It is of great significance to elucidate the mechanism of BPV increase. The cation channel transient receptor potential canonical 6 (TRPC6) is involved in a series of cardiovascular disease. Our experiment aimed to explore the role of TRPC6 in the development of BPV increase. Sino-aortic denervation (SAD) operation was applied to establish the model of BPV increase in rats. The BPV was presented as the standard deviation to the mean of systolic or diastolic blood pressure every 1 h during 12 h of the light period. SAD was performed in male Sprague Dawley (SD) rats at the age of 10 weeks. At 8 weeks after SAD operation, the hemodynamic parameters were determined non-invasively via a Rodent Blood Pressure Analysis System. The TRPC6 expressions in myocardial and thoracic aortic tissue was determined utilizing Western Blot, immunofluorescence and quantitative RT-PCR. The expression of TRPC3 was detected as well. To investigate whether TRPC6 was a causative factor of BPV increase in SAD rats, TRPC6 activator and inhibitor with three progressively increasing doses were intraperitoneally injected to the SAD rats. We found that SAD rats presented significant augmentation of systolic and diastolic BPV with no change of BP level and heart rate. The mRNA and protein expression levels of TRPC6 in myocardial and thoracic aortic tissue in SAD rats were substantially increased, but there was no obvious change in TRPC3 expression. The systolic and diastolic BPV increase were dose-dependently exacerbated after TRPC6 activation with GSK1702934A but were dose-dependently attenuated after TRPC6 inhibition with SAR7334. In Conclusion, the TRPC6 (but not TRPC3) expressions in myocardial and thoracic aortic tissue were substantially increased in SAD rats, and TRPC6 probably played an important role in the development of BPV elevation.
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