TRPV channels and vascular function

Transient receptor potential channels, of the vanilloid subtype (TRPV), act as sensory mediators, being activated by endogenous ligands, heat, mechanical and osmotic stress. Within the vasculature, TRPV channels are expressed in smooth muscle cells, endothelial cells, as well as in peri‐vascular ner...

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Bibliographic Details
Published in:Acta Physiologica 2011-09, Vol.203 (1), p.99-116
Main Authors: Baylie, R. L., Brayden, J. E.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cardiovascular System - metabolism
endothelium
Fundamental and applied biological sciences. Psychology
Hemodynamics - physiology
Humans
neurovascular
smooth muscle
TRPV Cation Channels - metabolism
TRPV channels
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Citations: Items that cite this one
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Summary:Transient receptor potential channels, of the vanilloid subtype (TRPV), act as sensory mediators, being activated by endogenous ligands, heat, mechanical and osmotic stress. Within the vasculature, TRPV channels are expressed in smooth muscle cells, endothelial cells, as well as in peri‐vascular nerves. Their varied distribution and polymodal activation properties make them ideally suited to a role in modulating vascular function, perceiving and responding to local environmental changes. In endothelial cells, TRPV1 is activated by endocannabinoids, TRPV3 by dietary agonists and TRPV4 by shear stress, epoxyeicosatrienoic acids (EETs) and downstream of Gq‐coupled receptor activation. Upon activation, these channels contribute to vasodilation via nitric oxide, prostacyclin and intermediate/small conductance potassium channel‐dependent pathways. In smooth muscle, TRPV4 is activated by endothelial‐derived EETs, leading to large conductance potassium channel activation and smooth muscle hyperpolarization. Conversely, smooth muscle TRPV2 channels contribute to global calcium entry and may aid constriction. TRPV1 and TRPV4 are expressed in sensory nerves and can cause vasodilation through calcitonin gene‐related peptide and substance P release as well as mediating vascular function via the baroreceptor reflex (TRPV1) or via increasing sympathetic outflow during osmotic stress (TRPV4). Thus, TRPV channels play important roles in the regulation of normal and pathological cellular function in the vasculature.
ISSN:1748-1708
1748-1716
DOI:10.1111/j.1748-1716.2010.02217.x