Capsaicin-Sensitive Sensory Nerves and the TRPV1 Ion Channel in Cardiac Physiology and Pathologies

Abstract

Cardiovascular diseases, including coronary artery disease, ischemic heart diseases such as acute myocardial infarction and postischemic heart failure, heart failure of other etiologies, and cardiac arrhythmias, belong to the leading causes of death. Activation of capsaicin-sensitive sensory nerves by the transient receptor potential vanilloid 1 (TRPV1) capsaicin receptor and other receptors, as well as neuropeptide mediators released from them upon stimulation, play important physiological regulatory roles. Capsaicin-sensitive sensory nerves also contribute to the development and progression of some cardiac diseases, as well as to mechanisms of endogenous stress adaptation leading to cardioprotection. In this review, we summarize the role of capsaicin-sensitive afferents and the TRPV1 ion channel in physiological and pathophysiological functions of the heart based mainly on experimental results and show their diagnostic or therapeutic potentials. Although the actions of several other channels or receptors expressed on cardiac sensory afferents and the effects of TRPV1 channel activation on different non-neural cell types in the heart are not precisely known, most data suggest that stimulation of the TRPV1-expressing sensory nerves or stimulation/overexpression of TRPV1 channels have beneficial effects in cardiac diseases.

Potential Interplay between Nrf2, TRPA1, and TRPV1 in Nutrients for the Control of COVID-19

“…Since oral capsaicin treatment cannot cause the increase in blood levels of capsaicin needed to act directly on cardiac or intravascular TRPV1 receptors, a remote activation should be suggested, which likely involves TRPV1 receptors localized on the capsaicin-sensitive sensory nerve terminals [ 87 ]. Indeed, experimental evidence proposes the protective roles of cardiac capsaicin-sensitive afferents and sensory TRPV1 receptors in myocardial protection through the release of sensory neuropeptides [ 88 ]. The chronic administration of systemic capsaicin induces sensory desensitization [ 89 ], leading to a model of Heart Failure with preserved Ejection Fraction (HFpEF).…”

The role of type 1 vanilloid receptors in protective and pathological mechanisms in the stomach under the action of ulcerogenic stimuli

“…Этот факт может объясняться тем, что, несмотря на генетическое устранение TRPV1-рецепторов, КЧН могут активироваться через другие рецепторы (Fukushima et al 2006) и вносить вклад в гастропротекцию. Более того, отсутствие TRPV1 может индуцировать экспрессию других рецепторов для компенсации их функциональной роли в клетке (Szabados et al 2020).…”

“…Послед-Н. И. Ярушкина, Т. Т. Подвигина, Л. П. Филаретова ние экспериментальные и клинические исследования свидетельствуют о том, что механизмы, связанные с TRPV1, могут иметь важное значение не только при лечении хронической боли, но и при лечении других патологических состояний, таких как рак, ожирение, кожные заболевания, сердечно-сосудистые заболевания (атеросклероз, гипертония) и диабет (Basharat et al 2020;Basith et al 2016;Brito et al 2014;Panchal et al 2018;Szabados et al 2020).…”

Early Lipid Raft-Related Changes: Interplay between Unilateral Denervation and Hindlimb Suspension

“…These channels are residents of lipid rafts in sensory neurons [ 29 ], and location of TRPV1 channels in the lipid rafts regulates functioning of these channels [ 29 , 30 ]. Caps administration leads to strong Na + and Ca 2+ influx through TRPV1, resulting the membrane depolarization, inactivation of voltage-dependent Na + channels and triggering multiple Ca 2+ -dependent events (i.e., exocytosis) [ 31 ]. Prolonged exposure to Caps can damage the TRPV1-expressing sensory neurons due to Ca 2+ overload [ 31 , 32 ].…”

“…Caps administration leads to strong Na + and Ca 2+ influx through TRPV1, resulting the membrane depolarization, inactivation of voltage-dependent Na + channels and triggering multiple Ca 2+ -dependent events (i.e., exocytosis) [ 31 ]. Prolonged exposure to Caps can damage the TRPV1-expressing sensory neurons due to Ca 2+ overload [ 31 , 32 ]. Since TRPV1 are preferentially localized to the Caps-sensitive primary afferents (CSPA), topical Caps application allows to selectively inhibit the function of CSPA [ 33 ].…”