An interesting article was published in the August 4th edition of Cell Metabolism. I'm always intrigued when common food ingredients are used to modulate biological systems. This article explores the effect of capsaicin on blood vessel tone. Capsaicin (or 8-methyl-N-vanillyl-6-nonenamide) is what makes "hot peppers" taste hot. This is achieved by activating a particular TRP channel (see Lisa's or Nate's prior post on TRP channels) called the TRPV1 channel. Capsaicin activates the TRPV1 channel and leads to an increase in intracellular calcium. This, in turn, causes the release of several neuropeptides such as substance P or calcitonin gene-related peptide. When a hot pepper in eaten, these changes in sensory nerves leads to the sensation of pain and local heat production.
What other tissue types express TRPV1 channels? And what role do these receptors play in patho- and physio-logical states? It has been previously demonstrated that TRPV1 channels are present in blood vessels. This study demonstrates the presence of TRPV1 in cultures endothelial cells as well as expression in the endothelial layer of an intact vessel. However, there have been a few often contradictory articles published about the acute actions of capsaicin on the blood pressure. Several investigators have shown a relaxing effect of capsaicin in various isolated vessels of pigs and rats. On the other hand, it has also been shown that TRPV1 activation causes vasoconstiction in vessels.
This study demonstrated that chronic TRPV1 activation by capsaicin led to enhanced production of the vasodilatory substance nitric oxide by endothelial cells. After performing several in vitro studies to verify this finding, the investigators fed spontaneous hypertensive rats a diet rich in capsaicin for 7 months and measured blood pressure. This led to a 15-20mmHg decrease in blood pressure as measured by radiotelemetry. However, this decrease in blood pressure was only evident after 4 months of treatment. An excellent editorial written by Dr. Sessa goes into more detail about this study. In conclusion, this is an interesting and provocative study. Much more research is needed before we can offer capsaicin as a therapy for hypertension. But, this could potentially lead to novel therapies aimed at activating the TRPV1 channel. It is still unclear exactly how capsaisin lowers blood pressure in SHR rats. It is likely that other systems are affected by chronic TRPV1 activation that can affect blood pressure. Such as the sympathetic nervous system or the renin-angiotensin system. For now, I'll keep enjoying my yearly hot pepper garden. I'll be interested to see where this research goes from here.
What other tissue types express TRPV1 channels? And what role do these receptors play in patho- and physio-logical states? It has been previously demonstrated that TRPV1 channels are present in blood vessels. This study demonstrates the presence of TRPV1 in cultures endothelial cells as well as expression in the endothelial layer of an intact vessel. However, there have been a few often contradictory articles published about the acute actions of capsaicin on the blood pressure. Several investigators have shown a relaxing effect of capsaicin in various isolated vessels of pigs and rats. On the other hand, it has also been shown that TRPV1 activation causes vasoconstiction in vessels.
This study demonstrated that chronic TRPV1 activation by capsaicin led to enhanced production of the vasodilatory substance nitric oxide by endothelial cells. After performing several in vitro studies to verify this finding, the investigators fed spontaneous hypertensive rats a diet rich in capsaicin for 7 months and measured blood pressure. This led to a 15-20mmHg decrease in blood pressure as measured by radiotelemetry. However, this decrease in blood pressure was only evident after 4 months of treatment. An excellent editorial written by Dr. Sessa goes into more detail about this study. In conclusion, this is an interesting and provocative study. Much more research is needed before we can offer capsaicin as a therapy for hypertension. But, this could potentially lead to novel therapies aimed at activating the TRPV1 channel. It is still unclear exactly how capsaisin lowers blood pressure in SHR rats. It is likely that other systems are affected by chronic TRPV1 activation that can affect blood pressure. Such as the sympathetic nervous system or the renin-angiotensin system. For now, I'll keep enjoying my yearly hot pepper garden. I'll be interested to see where this research goes from here.
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