Apart from modulating nociception, there is vital role of TRPV1 channels in modulating
atherosclerosis,
congestive heart failure, systemic
hypertension, pulmonary hypertension,
hemorrhagic shock and
vascular remodeling. TRPV1 channel activation has shielding effect against the development of
atherosclerosis and systemic
hypertension. TRPV1 channel activation alleviates the formation of atherosclerotic lesions via increasing the expression of
cholesterol efflux regulatory protein, UCP 2 and enhancing autophagy. Furthermore, activation of these channels enhances Na+ excretion and NO release to reduce the blood pressure. TRPV1 channel activation in the cardiac sensory neurons and subsequent CGRP release reduces
ischemia-reperfusion injury. Activation of these channels during conditioning enhances CGRP and SP release from the sensory nerve fibers innervating the heart to induce cardioprotection. However, activation of these channels may elicit detrimental effects in
pulmonary hypertension,
hemorrhage and
vascular remodeling. Activation of TRPV1 channels enhances smooth muscle cell proliferation to promote
pulmonary hypertension. Moreover, TRPV1 channel inhibition reduces massive
catecholamine release, improves survival during
hemorrhage. Activation of these channels enhances
vascular remodeling via enhancing NO release. Furthermore, dual role of TRPV1 channels has been reported in the perpetuation of
congestive heart failure. On one hand, TRPV1 channel activation increases the expression of UCP2,
PPAR- δ and mitochondrial
sirtuin 3 to decrease oxidative stress and reduce
heart injury. On the other hand, activation of these channels may enhance the expression of hypertrophic fibrotic
proteins viz. GATA4,
MMP to promote cardiac
fibrosis. The present review discusses the dual role of activation of TRPV1 channels in diseases associated with cardiovascular system.