Data associated with the publication: Cooling-induced cutaneous vasodilatation is mediated by small-conductance, calcium-activated potassium channels in tail arteries from male mice

We previously demonstrated that physiological cooling of cutaneous arteries causes dilation by increasing communication through myoendothelial gap junctions, which allows hyperpolarization initiated by the opening of endothelial calcium-activated potassium channels (KCa) to be conducted directly to the smooth muscle cells resulting in dilation. The goal of the present study was to determine the individual roles of endothelial KCa with small (SK3) and intermediate (IK1,SK4) conductance in this cooling induced dilation.

The study involved functional analyses to directly study the cooling-induced dilation, along with biochemical and immunofluorescent imaging analysis to evaluate the expression and localization of SK3 and IK1/SK4 channels. For functional analysis, vasomotor responses of mice isolated cutaneous tail arteries were analyzed by pressure myography at 37°C and 28°C. Cooling-induced dilation was assessed as the cooling-induced increase in endothelium-dependent dilation to acetylcholine and the cooling-induced inhibition of constrictor responses to U46619. The roles of SK3 and IK1/SK4 channels in the responses to cooling were assessed by evaluating the effects of selective pharmacological inhibition of SK3 (UCL1684) or IK1/SK4 (TRAM34). Expression of SK3 and IK1/SK4 was evaluated using immunoblot analysis of arterial lysates. Immunofluorescent analysis was performed by laser scanning microscopy on arterial segments to determine expression of SK3 and IK1/SK4 and their potential localization to holes in the internal elastic lamina, which is the site of myoendothelial junctions.