The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Activation of TRPV1 by Dietary Capsaicin Improves Endothelium-Dependent Vasorelaxation and Prevents Hypertension
Open accessAbstract
SUMMARY Some plant-based diets lower the cardiometabolic risks and prevalence of hypertension. New evidence implies a role for the transient receptor potential vanilloid 1 (TRPV1) cation channel in the pathogenesis of cardiometabolic diseases. Little is known about impact of chronic TRPV1 activation on the regulation of vascular function and blood pressure. Here we report that chronic TRPV1 activation by dietary capsaicin increases the phosphorylation of protein kinase A (PKA) and eNOS and thus production of nitric oxide (NO) in endothelial cells, which is calcium dependent. TRPV1 activation by capsaicin enhances endothelium-dependent relaxation in wild-type mice, an effect absent in TRPV1-deficient mice. Long-term stimulation of TRPV1 can activate PKA, which contributes to increased eNOS phosphorylation, improves vasorelaxation, and lowers blood pressure in genetically hypertensive rats. We conclude that TRPV1 activation by dietary capsaicin improves endothelial function. TRPV1-mediated increase in NO production may represent a promising target for therapeutic intervention of hypertension.
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Citations
Cites
The capsaicin receptor: a heat-activated ion channel in the pain pathway
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A Clinical Trial of the Effects of Dietary Patterns on Blood Pressure
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Impaired nociception and pain sensation in mice lacking the capsaicin receptor
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Molecular mechanisms of nociception
Julius, D., & Basbaum, A. I. (2001) · Nature · doi:10.1038/35093019 · Cited by 2,685 · cited 1×
“TRPV1 activation in sensory neurons causes nociception (Julius and Basbaum, 2001).”
BackgroundPrevalence, Awareness, Treatment, and Control of Hypertension Among United States Adults 1999–2004
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“Hypertension is a major risk factor for the increased incidence of stroke, coronary heart disease, and renal insufficiency (Ong et al., 2007).”
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Reciprocal Regulation of Endothelial Nitric-oxide Synthase by Ca2+-Calmodulin and Caveolin
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Cited by
Calcitonin Gene-Related Peptide: Physiology and Pathophysiology
Russell, F. A., King, R., Smillie, S.-J., Kodji, X., & Brain, S. D. (2014) · Physiological Reviews · doi:10.1152/physrev.00034.2013 · Cited by 1,258
Transient Receptor Potential Channels in the Vasculature
Earley, S., & Brayden, J. E. (2015) · Physiological Reviews · doi:10.1152/physrev.00026.2014 · Cited by 420
TRPV3 regulates nitric oxide synthase-independent nitric oxide synthesis in the skin
Miyamoto, T., Petrus, M. J., Dubin, A. E., & Patapoutian, A. (2011) · Nature Communications · doi:10.1038/ncomms1371 · Cited by 141
A Role for TRPV1 in Influencing the Onset of Cardiovascular Disease in Obesity
Marshall, N. J., Liang, L., Bodkin, J., Dessapt-Baradez, C., Nandi, M., Collot-Teixeira, S., Smillie, S.-J., Lalgi, K., Fernandes, E. S., Gnudi, L., et al. (2013) · Hypertension · doi:10.1161/hypertensionaha.112.201434 · Cited by 95
Phuong, T. T. T., Redmon, S. N., Yarishkin, O., Winter, J. M., Li, D. Y., & Križaj, D. (2017) · The Journal of Physiology · doi:10.1113/jp275052 · Cited by 91
Metadata
- Authors
- Yang, D., Luo, Z., Ma, S., Wong, W. T., Ma, L., Zhong, J., He, H., Zhao, Z., Cao, T., Yan, Z., Liu, D., Arendshorst, W. J., Huang, Y., Tepel, M., & Zhu, Z.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2010-08
- Volume
- 12
- Issue
- 2
- Pages
- 130-141
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W1969233157
- Cited by
- 349
- References
- 45
- FWCI
- 9.60
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Yang, D., Luo, Z., Ma, S., Wong, W. T., Ma, L., Zhong, J., He, H., Zhao, Z., Cao, T., Yan, Z., Liu, D., Arendshorst, W. J., Huang, Y., Tepel, M., & Zhu, Z. (2010). Activation of TRPV1 by Dietary Capsaicin Improves Endothelium-Dependent Vasorelaxation and Prevents Hypertension. Cell Metabolism. https://doi.org/10.1016/j.cmet.2010.05.015
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
