Cooling-Induced Dilatation of Cutaneous Arteries is Mediated by Increased Myoendothelial Communication.
Cooling-Induced Dilatation of Cutaneous Arteries is Mediated by Increased Myoendothelial Communication.
Am J Physiol Heart Circ Physiol. 2020 May 29;:
Authors: Flavahan S, Flavahan NA
Abstract
Cold exposure causes cutaneous vasoconstriction via a reflex increase in sympathetic activity and a local effect to augment adrenergic constriction. Local cooling also initiates cutaneous dilatation, which may function to restrain cold-induced constriction. However, the underlying mechanisms and physiological role of cold-induced dilatation have not been defined. Experiments were performed to assess the role of endothelial-derived mediators in this response. In isolated pressurized cutaneous mouse tail arteries, cooling (28oC) did not affect the magnitude of dilatation to acetylcholine in pre-constricted arteries. However, inhibition of NO (LNAME) and prostacyclin (PGI2)(indomethacin) reduced acetylcholine-induced dilatation at 37oC but not at 28oC, suggesting that cooling increased NO/PGI2-independent dilatation. This NO/PGI2-independent dilatation was reduced by inhibition of endothelial SK (UCL1684) and IK (TRAM34) Ca2+-activated K+-channels (KCa), consistent with endothelium-derived hyperpolarization (EDH). Cooling also increased dilatation to direct activation of KCa channels (SKA31,CyPPA), but did not affect dilatation to exogenous NO (DEA-NONOate). This cooling-induced increase in EDH-type dilatations was associated with divergent effect...
Source: American Journal of Physiology. Heart and Circulatory Physiology - Category: Physiology Authors: Flavahan S, Flavahan NA Tags: Am J Physiol Heart Circ Physiol Source Type: research