Abstract
Pressure-induced vasodilation (PIV) delays the decrease in cutaneous blood flow produced by local application of low pressure to the skin, a physiologically appropriate adjustment of local vasomotor function. Individuals without a normal PIV response have a high risk of ulceration. Here we demonstrate that acid-sensing ion channel 3 (Asic3) is an essential neuronal sensor for the vasodilation response to direct pressure in both humans and rodents and for protecting against pressure ulcers in mice.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acid Sensing Ion Channels / deficiency
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Acid Sensing Ion Channels / drug effects
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Acid Sensing Ion Channels / genetics
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Acid Sensing Ion Channels / physiology*
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Adult
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Amiloride / pharmacology
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Animals
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Calcitonin / antagonists & inhibitors
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Cnidarian Venoms / pharmacology
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Diclofenac / pharmacology
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / physiology
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Female
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Fingers / blood supply
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Humans
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Hyperemia / physiopathology*
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Ischemia / etiology
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Ischemia / physiopathology
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Male
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Mechanoreceptors / drug effects
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Mechanoreceptors / physiology*
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Mice
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Mice, Knockout
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Pressure / adverse effects
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Pressure Ulcer / etiology
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Pressure Ulcer / physiopathology*
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Pressure Ulcer / prevention & control
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Protein Precursors / antagonists & inhibitors
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Random Allocation
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Rats
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Rats, Wistar
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Single-Blind Method
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Skin / blood supply*
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Vasodilation / physiology*
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Young Adult
Substances
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APETx2 protein, Anthopleura elegantissima
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ASIC3 protein, human
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ASIC3 protein, mouse
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ASIC3 protein, rat
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Acid Sensing Ion Channels
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Cnidarian Venoms
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Protein Precursors
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Diclofenac
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Amiloride
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Calcitonin