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Blood Circulation Stimulation Properties of Cayenne Pepper:A Review



Cayenne pepper (also called Capsicum frutescence) is a stimulating herb made from the dried pods of chili peppers and is well known for its pungent taste and smell. Cayenne is a popular spice used in many different regional styles of cooking, but it has also been used medicinally for thousands of years. Cayenne is often referred to as chili, which is the Aztec name for cayenne pepper. The main medicinal properties of cayenne are derived from a chemical called capsaicin. Capsaicin is the ingredient which gives peppers their HEAT. A pepper's capsaicin content ranges from 0-1.5%. Peppers are measured according to heat units. The degree of heat determines the peppers' usage and value. Generally, the hotter the pepper, the more capsaicin it contains. In addition to adding heat to the pepper, capsaicin acts to reduce platelet stickiness and relieve pain. Other constituents of cayenne are vitamins E, vitamin C and carotenoids. Today cayenne is used worldwide to treat a variety of health conditions, including poor Circulation, weak digestion, heart disease, chronic pain, sore throats, headache sand toothache Cayenne is the greatest herbal aid to circulation and can be used on a regular basis. Dr. Richard Schulze, the medical herbalist, says that "If you master only one herb in your life, master Cayenne pepper. It is more powerful than any other
IOSR Journal of Applied Chemistry (IOSR-JAC)
e-ISSN: 2278-5736.Volume 11, Issue 5 Ver. I (May. 2018), PP 78-83
DOI: 10.9790/5736-1105015743 78|Page
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
MukulChauhan, Chhavi Kant, ChitraNegi And PrachiChauhanDepartment of chemistry,
School of Applied Science ShriVenkateshwara University, Gajraula, U.P. , IndiaCorresponding
Author:MukulChauhan, Chhavikant
Abstract: Cayenne pepper (also called Capsicum frutescence) is a stimulating herb made from the dried pods of
chili peppers and is well known for its pungent taste and smell. Cayenne is a popular spice used in many different
regional styles of cooking, but it has also been used medicinally for thousands of years. Cayenne is often referred to
as chili, which is the Aztec name for cayenne pepper. The main medicinal properties of cayenne are derived from a
chemical called capsaicin. Capsaicin is the
ingredient which gives peppers their HEAT. A pepper's capsaicin content ranges from 0-1.5%. Peppers are
measured according to heat units. The degree of heat determines the peppers' usage and value. Generally, the hotter
the pepper, the more capsaicin it contains. In addition to adding heat to the pepper, capsaicin acts to reduce platelet
stickiness and relieve pain. Other constituents of cayenne are vitamins E, vitamin C and carotenoids. Today cayenne
is used worldwide to treat a variety of health conditions, including poor Circulation, weak digestion, heart disease,
chronic pain, sore throats, headache sand toothache Cayenne is the greatest herbal aid to circulation and can be
used on a regular basis. Dr. Richard Schulze, the medical herbalist, says that "If you master only one herb in your
life, master Cayenne pepper. It is more powerful than any other."
Date of Submission:15-05-2018 Date of acceptance:21-05-2018
Cayenne pepper belongs to the capsicum family, and its botanical name is capsicumannuum. It is the red chili
pepperthat is used to add flavor in food and has high medicinal values.Cayenne contains vitamin E, vitamin C,
vitamin K, carotenoids, and the complete B complex vitamins. It is also a source of organic calcium, potassium,
manganese, and dietary fiber.For health and medicinal purposes, you only need to drink small amounts of cayenne
powder, mixed in a glass of water.[1-2]
Risk factors for cardiovascular disease (CVD) include metabolic and vascular factors, such as hypercholesterolemia,
hyperglycaemia, hyperinsulinemia, obesity, hypertension and arterial stiffness. One approach to reducing CVD risk
is to reduce body weight. Obesity elevates the risk of hyperglycaemia, hyperinsulinemia, and vascular resistance
(Eckel et al., 2005; Moller and Kaufman, 2005; Sundell, 2005). Decreasing energy input and increasing energy
output (e.g., low energy diets and increasing exercise) are the two approaches for weight reduction. Chilli or its
active component capsaicin has been shown to increase energy expenditure and/or fat oxidation (in animals and
humans) and lower serum lipids (in animals).[3-5]
How cayenne pepper can helps us
Cayenne pepper increases blood circulation. It also draws the blood to where it is especially needed.
Because of these special abilities, it can be used to help you in many ways. Cayenne is a counterirritant; it brings
blood to the surface and allows the toxins to be taken away. It wonderfully improves blood circulation[.7]
The benefits of cayenne are almost too unbelievable; but its reputation keeps growing and growing, and deservedly
so. It can do everything from killing cancer cells in the prostate, lungs, and pancreas to immediately stopping a heart
attack within 30 seconds. Incredible, but successful in many instances. The health benefits of cayenne pepper
include improvements in regard to digestion, immunity, heart diseases, dyspepsia, inflammation, headache, throat
congestion, and blood circulation. Cayenne pepper improves the effectiveness of other herbs.[8-11]
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
DOI: 10.9790/5736-1105015743 79|Page
Prevents heart attack
There are evidences that prove that giving cayenne extract orally, to a patient, helps to stop heart attack.
Cayenne helps to reduce cholesterol levels in the blood. Cayenne helps to dissolve fibrin, which causes formation of
blood clots. It also reduces triglyceride levels. It is excellent for any type of internal hemorrhage.Cayenne pepper
increases metabolism by immediately speeding up the flow of blood in the arteries and veins.[15-16].
This herb is a great food for the circulatory system. It feeds the necessary elements into the cell structure of
the arteries, veins, and capillaries; so that these regain the elasticity of youth again, and the blood pressure adjusts
itself to normal.
It improves blood circulation. When any body part is sick, the blood flow to that area is usually affected. Cayenne
helps to remove entire blood congestion, stimulates the blood flow, makes sure that the vitamins are properly
delivered to all areas, and waste is removed.[13-14]
Dr. John Christopher, the famed natural herbalist, was relentlessly harassed by the government for his practice of
herbal medicine, all the while assisting patients in curing heart disease, cancer, tuberculosis, infertility, rheumatism,
leukemia, and many other conditions with herbs. He could instantly stop a heart attack if he could get the patient to
drink a glass of warm cayenne water. He said, “A teaspoon of cayenne should bring the patient out of the heart
attack.” For internal hemorrhaging (bleeding inside the body), if the patient can drink a glass of extra warm cayenne
water, Dr. Christopher wrote, “by the count of ten the bleeding will stop. Instead of all the pressure being
centralized, it is equalized and the clotting
becomes more rapid.” With over 700,000 Americans experiencing a stroke each year and almost half a million dying
yearly of either heart disease or related issues, cayenne pepper is worth keeping on your shelf. Capsicum may be
valuable in the prevention and treatment of blood clots. Cayenne is also great for heartburn.[19-22]
Healing the sick part of body
When you have a sick area, there ‘soften a restriction of blood flow to that area. Blood flow is what takes
nutrition and the healing properties of herbs to those cells. Blood flow is also what Carries out and removes waste
material. Cayenne pepper is like TNT. It blasts through all that blockage to get to that area which is sick, taking with
it all the minerals and vitamins from the Foods you eat, and all the vital chemicals from the herbs you take-all the
way to the sick area.
Cayenne pepper is usually labeled 40,000, 60,000, 90,000 or more heat units. Generally, the higher the number of
heat units, the more beneficial. The lower-heat cayenne peppers are a lot less efficient, and they are the ones which
are most highly contaminated. These are the ones you see labeled for 30,000 heat units. These are the ones to stay
away from.[25-27]
Use of cyanne powder in place of capsule
It is recommended that the cayenne powder be used, as opposed to capsules. It is believed that you are only
getting a small part of the potential effect of cayenne pepper by taking it in capsules. When you put cayenne in your
mouth, your stomach secretes digestive juices before the cayenne ever gets there. So when the cayenne gets down
there, your stomach is ready for it.
But if you swallow a capsule, your tongue tastes nothing. A capsule goes down in your stomach, and your stomach
notices nothing, at first. Then, 5minutes later the gelatin bursts, and you have a ½ tea spoon of cayenne pepper in
your stomach and your body is shocked. You surprised it. What is going on is that some of cayenne's healing action
occurs right in your mouth. As cayenne touches your tongue, the cayenne absorbs in seconds and nerve endings send
signals throughout the body-sending waves of fresh blood throughout your body.[32-37]
Controlls high blood pressure and regulates the temperature of body
Cayenne pepper for high blood pressure is certainly one of its core uses; but cayenne cleans the arteries as
well, helping to rid the body of the bad LDL cholesterol and triglycerides. It is an excellent home treatment for mild
high blood pressure and high blood cholesterol levels. [42]
Cayenne preparations prevent platelets from clumping together and accumulating in the blood, allowing the blood to
flow more easily. Since it is thought to help improve circulation, it’s often used by those who have cold hands and
feet. It equalizes the blood circulation in the arterial and venous system, and produces natural warmth in your body.
It does this by regulating the flow of blood from the head to the feet, so that the pressure is equalized. It
influencesthe heart immediately; then it gradually extends its effects to the arteries, capillaries, and nerves.[39-41]
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
DOI: 10.9790/5736-1105015743 82|Page
Avoid use of cayenne in case of
Keep in mind that regularly taking large amounts of cayenne may eventually damage the kidneysand
lead to pleurisy and other conditions caused by weakened kidney function. It is the kidneys which have to process
the cayenne by extracting it from the blood into the urine. Too much cayenne, too frequently, weakens kidney
function. If you’ve ever accidentally rubbed your eyes after cutting hot peppers, you know this herb should be
handled carefully. Cayenne pills may cause a burning sensation in the throat, stomach, or rectum of sensitive
individuals. Some people may tolerate cayenne fluid preparations or combination products better than tablets or
capsules. Others may find cayenne pepper in the diet easier to digest than cayenne medications. Only use small,
cautious doses. Avoid getting cayenne into the eyes or open wounds. Do not use topical applications of cayenne
products too frequently; since there is some concern that nerve damage could occur with daily repetitive use.
Cayenne placed directly on the skin can cause burns and even blisters; so dilute a cayenne preparation in oil before
placing it on the skin. Or mix it with flour and water until it forms a paste, which you can spread on muslin, to
prepare a poultice. You also can mix cayenne with orrisroot powder and dust it very lightly on heavily oiled skin,
working it in with massage.[45-49]
Do not use cayenne in cases of high fever (104 degrees Fahrenheit or above). Cayenne preparations are not
recommended for use by individuals who have rapid heart rates or who become overheated or perspire easily. Avoid
internal use of cayenne in cases of asthma and gastrointestinal irritation or inflammation, except under the
supervision of an experienced herbalist. Do not use cayenne on broken skin. Like all other foods or herbs, we have
to also be careful when using this herb. Excessive consumption may cause burning sensations in the throat, stomach,
or rectum. When cooking or making medicines with cayenne peppers, you must take into account the widely varying
intensities (heat) of different peppersfrom very mild to extremely fiery.[50-51]
Cancer and detoxification
Cayenne pepper is also very well known for its cancer fighting properties. It may prevent the spread of
cancerous cells, while initiating apoptosis or programmed cell death. In lab studies, cayenne was able to kill
prostate, breast, stomach, pancreas and lung cancer. [17-19]
However, the question is, would it work on us?
Due to benefits of cayenne pepper, herb is also used in detoxification formulas since it exhibits anti- bacterial, anti-
viral and anti- fungal properties. Capsaicin from cayenne is very well absorbed from the digestive track into the
blood stream. On the other hand, it is questionable how much should we consume, in order to experience cayenne
benefits and avoid the side effects.[53-55]
Side effects
Possible side effects include nausea, vomiting, stomachaches and diarrhea. When applied to the skin and
left for some time, the herb will provoke burning reaction. This is especially dangerous, if cayenne comes in contact
with eyes. Higher doses of cayenne may lead to kidney and liver damage, severe gastrointestinal problems
And even death. Besides capsaicin, the herb contains other flavonoids, too, which may be Carcinogenic in high
Blood Circulation Stimulation Properties of Cayenne Pepper:A Review
DOI: 10.9790/5736-1105015743 82|Page
Chemical composition
Ca .26%
albumen 2.4%
p .09
pectin 2.33
K .17
gums 1.3
Na tr
starch 2.0
CI tr
capsaicin .43
Mg .31
capsacutin oil 16.35
Fe .0006
pentosans totaling 8.59 solaine
xanthenes .82
Cu tr
oleic acid
Zn tr
palmitic acid 1.85
Carotene-various carotenoid pigment.
no carotene
steanc acid
A 12,137 Mg/Ib
fatty acids
B-1 78
B-2 12
C (ascorbic acid) 493
Cayenne is cheap and easily available herb found in supermarkets. You can use it to destroy blood clots, improve
lipid profiles, heart function and above all, circulation. However, it is also used for treating viral infections such as
shingles and herpes, arthritis, diabetes, muscle pain, as well as for relieving pain associated with gum disease and
headaches. For which ever reason you decide to get you some benefits of cayenne pepper, don't go overboard. Too
much capsaicin can be counterproductive.
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MukulChauhan, Chhavi Kant "Blood Circulation Stimulation Properties of Cayenne Pepper:A
Review." IOSR Journal of Applied Chemistry (IOSR-JAC) 18.5(2018): 01-06.
IOSR Journal of Applied Chemistry (IOSR-JAC) is UGC approved Journal with Sl. No. 4152,
Journal no. 46132.
... The pepper's high nutritional value results in high year-round demand on the market. Pepper fruits are used as a dried powder in salads, pickles, filling, sauces, and sauce (Mukul et al.,2018;Toyer, 2021). ...
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High-salt diet-induced cardiac hypertrophy and fibrosis are associated with increased reactive oxygen species production. Transient receptor potential vanilloid type 1 (TRPV1), a specific receptor for capsaicin, exerts a protective role in cardiac remodeling that resulted from myocardial infarction, and peroxisome proliferation-activated receptors δ (PPAR-δ) play an important role in metabolic myocardium remodeling. However, it remains unknown whether activation of TRPV1 could alleviate cardiac hypertrophy and fibrosis and the effect of cross-talk between TRPV1 and PPAR-δ on suppressing high-salt diet-generated oxidative stress. In this study, high-salt diet-induced cardiac hypertrophy and fibrosis are characterized by significant enhancement of HW/BW%, LVEDD, and LVESD, decreased FS and EF, and increased collagen deposition. These alterations were associated with downregulation of PPAR-δ, UCP2 expression, upregulation of iNOS production, and increased oxidative/nitrotyrosine stress. These adverse effects of long-term high-salt diet were attenuated by chronic treatment with capsaicin. However, this effect of capsaicin was absent in TRPV1(-/-) mice on a high-salt diet. Our finding suggests that chronic dietary capsaicin consumption attenuates long-term high-salt diet-induced cardiac hypertrophy and fibrosis. This benefit effect is likely to be caused by TRPV1 mediated upregulation of PPAR-δ expression.
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TRPV1 is expressed in sensory neurons and vascular smooth muscle cells, contributing to both pain perception and tissue blood distribution. Local desensitization of TRPV1 in sensory neurons by prolonged, high dose stimulation is re-engaged in clinical practice to achieve analgesia, but the effects of such treatments on the vascular TRPV1 are not known. Newborn rats were injected with capsaicin for five days. Sensory activation was measured by eye wiping tests and plasma extravasation. Isolated, pressurized skeletal muscle arterioles were used to characterize TRPV1 mediated vascular responses, while expression of TRPV1 was detected by immunohistochemistry. Capsaicin evoked sensory responses, such as eye wiping (3.6±2.5 versus 15.5±1.4 wipes, p<0.01) or plasma extravasation (evans blue accumulation 10±3 versus 33±7 µg/g, p<0.05) were reduced in desensitized rats. In accordance, the number of TRPV1 positive sensory neurons in the dorsal root ganglia was also decreased. However, TRPV1 expression in smooth muscle cells was not affected by the treatment. There were no differences in the diameter (192±27 versus 194±8 µm), endothelium mediated dilations (evoked by acetylcholine), norepinephrine mediated constrictions, myogenic response and in the capsaicin evoked constrictions of arterioles isolated from skeletal muscle. Systemic capsaicin treatment of juvenile rats evokes anatomical and functional disappearance of the TRPV1-expressing neuronal cells but does not affect the TRPV1-expressing cells of the arterioles, implicating different effects of TRPV1 stimulation on the viability of these cell types.
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The transient receptor potential vanilloid type 1 (TRPV1) is crucial in the pathogenesis of atherosclerosis; yet its role and underlying mechanism in the formation of macrophage foam cells remain unclear. Here, we show increased TRPV1 expression in the area of foamy macrophages in atherosclerotic aortas of apolipoprotein E-deficient mice. Exposure of mouse bone-marrow-derived macrophages to oxidized low-density lipoprotein (oxLDL) upregulated the expression of TRPV1. In addition, oxLDL activated TRPV1 and elicited calcium (Ca(2+)) influx, which were abrogated by the pharmacological TRPV1 antagonist capsazepine. Furthermore, oxLDL-induced lipid accumulation in macrophages was ameliorated by TRPV1 agonists but exacerbated by TRPV1 antagonist. Treatment with TRPV1 agonists did not affect the internalization of oxLDL but promoted cholesterol efflux by upregulating the efflux ATP-binding cassette (ABC) transporters ABCA1 and ABCG1. Moreover, the upregulation of ABC transporters was mainly through liver X receptor α - (LXR α -) dependent regulation of transcription. Moreover, the TNF- α -induced inflammatory response was alleviated by TRPV1 agonists but aggravated by the TRPV1 antagonist and LXR α siRNA in macrophages. Our data suggest that LXR α plays a pivotal role in TRPV1-activation-conferred protection against oxLDL-induced lipid accumulation and TNF- α -induced inflammation in macrophages.
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Background Diabetic cardiovascular complications are characterised by oxidative stress-induced endothelial dysfunction. Uncoupling protein 2 (UCP2) is a regulator of mitochondrial reactive oxygen species (ROS) generation and can antagonise oxidative stress, but approaches that enhance the activity of UCP2 to inhibit ROS are scarce. Our previous studies show that activation of transient receptor potential vanilloid 1 (TRPV1) by capsaicin can prevent cardiometabolic disorders. In this study, we conducted experiments in vitro and in vivo to investigate the effect of capsaicin treatment on endothelial UCP2 and oxidative stress. We hypothesised that TRPV1 activation by capsaicin attenuates hyperglycemia-induced endothelial dysfunction through a UCP2-mediated antioxidant effect. Methods TRPV1-/-, UCP2 -/- and db/db mice, as well as matched wild type (WT) control mice, were included in this study. Some mice were subjected to dietary capsaicin for 14 weeks. Arteries isolated from mice and endothelial cells were cultured. Endothelial function was examined, and immunohistological and molecular analyses were performed. Results Under high-glucose conditions, TRPV1 expression and protein kinase A (PKA) phosphorylation were found to be decreased in the cultured endothelial cells, and the effects of high-glucose on these molecules were reversed by the administration of capsaicin. Furthermore, high-glucose exposure increased ROS production and reduced nitric oxide (NO) levels both in endothelial cells and in arteries that were evaluated respectively by dihydroethidium (DHE) and DAF-2 DA fluorescence. Capsaicin administration decreased the production of ROS, restored high-glucose-induced endothelial dysfunction through the activation of TRPV1 and acted in a UCP2-dependent manner in vivo. Administration of dietary capsaicin for 14 weeks increased the levels of PKA phosphorylation and UCP2 expression, ameliorated the vascular oxidative stress and increased NO levels observed in diabetic mice. Prolonged dietary administration of capsaicin promoted endothelium-dependent relaxation in diabetic mice. However, the beneficial effect of capsaicin on vasorelaxation was absent in the aortas of UCP2 -/- mice exposed to high-glucose levels. Conclusion TRPV1 activation by capsaicin might protect against hyperglycemia-induced endothelial dysfunction through a mechanism involving the PKA/UCP2 pathway.
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Nonalcoholic fatty liver is characterized by the fatty deformation and lipid deposition of hepatic parenchymal cells that are associated with cardiometabolic diseases. In this study, we report the effect of capsaicin on its receptor, transient receptor potential vanilloid 1 (TRPV1) cation channel, in preventing fatty liver formation. Functional TRPV1 has been detected in hepatocytes and liver tissues. TRPV1 activation by capsaicin reduced lipid accumulation and triglyceride level in the liver from wild-type (WT) mice. However, these effects were absent in the liver from TRPV1(-/-) mice. Chronic dietary capsaicin increased the hepatic uncoupling protein 2 (UCP2) expression in WT but not in TRPV1(-/-) mice (P < 0.01). We conclude that TRPV1 long-time activation might prevent high-fat diet-induced fatty liver in mice through upregulation of hepatic UCP2. Dietary capsaicin may represent a promising intervention in populations at high risk for fatty liver.
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Activation of transient receptor potential vanilloid type-1 (TRPV1) channels may affect lipid storage and the cellular inflammatory response. Now, we tested the hypothesis that activation of TRPV1 channels attenuates atherosclerosis in apolipoprotein E knockout mice (ApoE(-/-)) but not ApoE(-/-)TRPV1(-/-) double knockout mice on a high-fat diet. Both TRPV1 mRNA and protein expression were identified in vascular smooth muscle cells (VSMC) and in aorta from C57BL/6J mice using RT-PCR, immunoblotting, and immunohistochemistry. In vitro, activation of TRPV1 by the specific agonists capsaicin and resiniferatoxin dose-dependently increased cytosolic calcium and significantly reduced the accumulation of lipids in VSMC from C57BL/6J mice but not from TRPV1(-/-) mice. TRPV1 activation increased ATP-binding cassette transporter A1 (ABCA1) expression and reduced low-density lipoprotein-related protein 1 (LRP1) expression in VSMC by calcium-dependent and calcineurin- and protein kinase A-dependent mechanisms. These results showed increased cellular cholesterol efflux and reduced cholesterol uptake. In vivo, long-term activation of TRPV1 by capsaicin for 24 weeks increased ABCA1 and reduced LRP1 expression in aorta from ApoE(-/-) mice on a high-fat diet. Long-term activation of TRPV1 significantly reduced lipid storage and atherosclerotic lesions in the aortic sinus and in the thoracoabdominal aorta from ApoE(-/-) mice but not from ApoE(-/-)TRPV1(-/-) mice on a high-fat diet. These findings indicated that TRPV1 activation ameliorates high-fat diet-induced atherosclerosis. Activation of TRPV1 may be a novel therapeutic tool to attenuate atherosclerosis caused by a high-fat diet.
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Previous studies show that endothelial nitric oxide synthase (eNOS) plays a prominent role in maintaining cerebral blood flow and preventing stroke. Capsaicin in hot pepper can increase the phosphorylation of eNOS in endothelial cells. We test the hypothesis that chronic dietary capsaicin can prevent stroke through activation of cerebrovascular transient receptor potential vanilloid 1 (TRPV1) channels in stroke-prone spontaneously hypertensive rats (SHRsp). SHRsp were fed dietary capsaicin, and their onset of stroke was examined. TRPV1 knockout and transgenic mice were used for determining the function of TRPV1 channels. Expression of eNOS and cerebrovascular reactivity were examined. Immunofluorescence showed TRPV1 channels and eNOS coexpression in cerebral arterioles. Administration of capsaicin significantly increased phosphorylated eNOS in carotid arteries from wild-type mice but not in TRPV1 knockout mice. Inhibition of eNOS using N(G)-nitro-L-arginine methyl ester, removal of endothelium, or mutant TRPV1 significantly reduced capsaicin-induced endothelium-dependent relaxation of basilar arteries in mice. Chronic dietary capsaicin also remarkably increased eNOS expression in carotid arteries from SHRsp. Compared with Wistar-Kyoto rats, SHRsp had impaired endothelium-dependent relaxation of basilar arteries. Administration of capsaicin or L-arginine significantly improved the endothelium-dependent relaxation of basilar arteries in SHRsp. SHRsp had hypertrophy of cerebral arterioles, which was reversed by dietary capsaicin. Importantly, long-term administration of capsaicin significantly delayed the onset of stroke and increased the survival time in SHRsp. Activation of TRPV1 channels by dietary capsaicin mediated increases in phosphorylation of eNOS and could represent a novel target for dietary intervention of stroke.
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Vanilloid agonists (capsaicin, resiniferatoxin, [RTX]) applied to the peripheral nerves provide conduction blockade. In contrast to the analgesic component of conduction anesthesia produced by local anesthetics, vanilloid agonists provide conduction analgesia not associated with suppression of motor or sensory functions not related to pain. Vanilloid agonists provide conduction analgesia selectively because their effect on the nerve trunks is limited to C- and ADelta-fibers. RTX is much more potent than capsaicin and has a wider therapeutic window. In rat experiments, perineural RTX produced a long-lasting thermal and mechanical hypoalgesia with a very wide separation between effective concentrations (from 0.00003% to 0.001%) providing an effect lasting from several hours to several weeks. A nerve block with RTX prevented the development of thermal and mechanical hyperalgesia as well as pain behavior in a model of incisional pain. RTX-induced conduction blockade has an inherent drawback of TRPV1 agonists, the initial excitation (pain); therefore, a local anesthetic should be injected to prevent it. When RTX was applied to the rat's sciatic nerve in doses necessary to provide conduction analgesia, the frequency of unmyelinated fiber degeneration was more than an order of magnitude lower than that with the therapeutic concentration of lidocaine. These promising results should be confirmed by experiments in species other than rodents (pigs, sheep). Taken together, the data indicate possible clinical applicability of vanilloid-induced conduction analgesia.
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We investigated the molecular mechanism underlying the role of transient receptor potential vanilloid type 1 (TRPV1), a Ca(2+)-permeable non-selective cation channel, in the activation of endothelial nitric oxide (NO) synthase (eNOS) in endothelial cells (ECs) and mice. In ECs, TRPV1 ligands (evodiamine or capsaicin) promoted NO production, eNOS phosphorylation, and the formation of a TRPV1-eNOS complex, which were all abrogated by the TRPV1 antagonist capsazepine. TRPV1 ligands promoted the phosphorylation of Akt, calmodulin-dependent protein kinase II (CaMKII) and TRPV1, and increased the formation of a TRPV1-Akt-CaMKII complex. Removal of extracellular Ca(2+) abolished the ligand-induced increase in the phosphorylation of Akt and CaMKII, formation of a TRPV1-eNOS complex, and eNOS activation. Inhibition of PI3K and CaMKII suppressed the ligand-induced increase in TRPV1 phosphorylation, formation of a TRPV1-eNOS complex, and eNOS activation. TRPV1 activation increased the phosphorylation of Akt, CaMKII, and eNOS in the aortas of wild-type mice but failed to activate eNOS in TRPV1-deficient aortas. Additionally, TRPV1 ligand-induced angiogenesis was diminished in eNOS- or TRPV1-deficient mice. When compared with apolipoprotein E (ApoE)-deficient mice, ApoE/TRPV1-double-knockout mice displayed reduced phosphorylation of eNOS, Akt, and CaMKII in aortas but worsened atherosclerotic lesions. TRPV1 activation in ECs may trigger Ca(2+)-dependent PI3K/Akt/CaMKII signalling, which leads to enhanced phosphorylation of TRPV1, increased TRPV1-eNOS complex formation, eNOS activation and, ultimately, NO production.
High salt (HS) intake contributes to the development of hypertension. Epithelial sodium channels play crucial roles in regulating renal sodium reabsorption and blood pressure. The renal transient receptor potential vanilloid 1 (TRPV1) cation channel can be activated by its agonist capsaicin. However, it is unknown whether dietary factors can act on urinary sodium excretion and renal epithelial sodium channel (ENaC) function. Here, we report that TRPV1 activation by dietary capsaicin increased urinary sodium excretion through reducing sodium reabsorption in wild-type (WT) mice on a HS diet but not in TRPV1(-/-) mice. The effect of capsaicin on urinary sodium excretion was involved in inhibiting αENaC and its related with-no-lysine kinase 1/serum- and glucocorticoid-inducible protein kinase 1 pathway in renal cortical collecting ducts of WT mice. Dietary capsaicin further reduced the increased αENaC activity in WT mice attributed to the HS diet. In contrast, this capsaicin effect was absent in TRPV1(-/-) mice. Immunoprecipitation study indicated αENaC specifically coexpressed and functionally interact with TRPV1 in renal cortical collecting ducts of WT mice. Additionally, ENaC activity and expression were suppressed by capsaicin-mediated TRPV1 activation in cultured M1-cortical collecting duct cells. Long-term dietary capsaicin prevented the development of high blood pressure in WT mice on a HS diet. It concludes that TRPV1 activation in the cortical collecting ducts by capsaicin increases urinary sodium excretion and avoids HS diet-induced hypertension through antagonizing αENaC-mediated urinary sodium reabsorption. Dietary capsaicin may represent a promising lifestyle intervention in populations exposed to a high dietary salt intake.