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Lee Swanson Research Update
Chili Compound Linked to Lower Blood Pressure
August 2010
A new study has linked frequent intake of capsaicin to a reduction
in blood pressure, the first time that the effect has been observed for
long-term use.
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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