Editors' ChoiceHypertension

Hot Peppers to Cool Blood Pressure

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Science Translational Medicine  18 Aug 2010:
Vol. 2, Issue 45, pp. 45ec128
DOI: 10.1126/scitranslmed.3001567

Capsaicin is the compound that makes jalapeño peppers “hot,” inducing a burning sensation when it touches one’s mouth, eyes, or skin. This substance exerts its effects by activating a receptor—the transient receptor potential vanilloid 1 (TRPV1) channel—located on pain- and heat-sensing neurons. Capsaicin binding to TRPV1 triggers an increase in intracellular calcium and the release of several neuropeptides. Prolonged exposure promotes analgesia via desensitization of sensory nerves, which is the basis for capsaicin’s use in over-the-counter analgesic skin creams. Now, a study by Yang et al. identifies a new potential use of capsaicin: as a blood pressure–lowering treatment.

The most important observation of the study is that prolonged feeding of capsaicin (at a concentration of 0.02%—a lot of heat) to rodent models of hypertension lowers blood pressure. This effect is dependent on TRPV1, because capsaicin did not reduce blood pressure in mice that lacked TRPV1. The authors showed that TRPV1 is expressed in endothelial cells (which line blood vessels); furthermore, capsaicin increases the phosphorylation of protein kinase A (PKA) and endothelial nitric oxide synthase (eNOS) in a TRPV1-dependent fashion in endothelium or endothelial cells, thus increasing production of nitric oxide, which is a key mediator of vascular relaxation.

What remains unclear, however, is whether these effects in endothelial cells are responsible for the long-term in vivo effects of capsaicin. According to Unigene of the National Center for Biotechnology Information, TRPV1 is expressed in many human tissues, including kidney, brain, and immune cells; all of these organs regulate blood pressure. That capsaicin has indirect effects on the endothelium and on blood pressure is supported by the authors’ observation that capsaicin has no acute effects on either blood pressure, PKA, or eNOS activation even after 3 weeks of treatment in mice; only after 4 months of capsaicin feeding was an effect on blood pressure apparent. This study provides a rationale for human trials targeting TRPV1, even if it is likely that one needs to “take the heat” for many months to cool one’s blood pressure.

D. Yang et al., Activation of TRPV1 by dietary capsaicin improves endothelium-dependent vasorelaxation and prevents hypertension. Cell Metab. 12, 130–141, 2010. [Abstract]

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