Chili Compound Linked to Lower Blood Pressure
Lee Swanson Research Update
The study provides fresh evidence to support the theory that capsaicin can improve blood vessel function and lower blood pressure, which lends support to its use as a dietary supplement or functional ingredient in foods.
Published in the journal Cell Metabolism, the study suggests that the blood vessel receptor TRPV1 is stimulated by capsaicin, mediating a beneficial effect in the cardiovascular system by promoting nitric oxide release and lowering blood pressure.
The researchers, led by Zhiming Zhu from Third Military Medical University in China, wrote: "TRPV1 activation through dietary capsaicin may represent a promising intervention of lifestyle in high-risk populations with hypertension and related vascular disorders."
Capsaicin is found in the white pulp of chili peppers and is the compound that gives them their "heat," causing a burning sensation in any tissue it comes into contact with. The burning pain caused by capsaicin is due to its selective binding of capsaicin to the receptor TRPV1.
Transient receptor potential channels (TRPs), including TRPV1, have been linked with the development of several diseases, including cardiovascular and neurological diseases, asthma, cancer and renal disease.
The new study is not the first to look for a molecular link between capsaicin and lower blood pressure, but earlier studies were based on short-term exposure to the compound.
The research assigned transgenic mice and rats to one of two groups (control or capsaicin) and assessed various cardiovascular risk factors (such as blood pressure and nitric oxide levels) over a six-month period.
The results of the study provide experimental evidence for the beneficial effects of dietary capsaicin in reducing high blood pressure via direct stimulation of TRPV1 channels.
The researchers’ observations suggest that TRPV1 activation may increase the activity of endothelial nitric oxide synthase (eNOS) in arteries and increase nitric oxide (NO) production in endothelial cells.
The study’s findings suggest that TRPV1 activation is required to enhance eNOS activity, however the researchers also state that there is no way to exclude the possibility that other mechanisms may also contribute to the up-regulation of eNOS activity during prolonged capsaicin consumption.
The researchers stated: "Present results agree with other reports showing that TRPV1 activation causes relaxation of isolated arteries."
Cell Metabolism Published online ahead of print.
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August 2010