Na+/K+-ATPase plays a major role in mediating cutaneous thermal hyperemia achieved by local skin heating to 39 ºC.

Abstract

Na+/K+-ATPase is integrally involved in mediating cutaneous vasodilation during an exercise-heat stress, which includes an interactive role with nitric oxide synthase (NOS). Here, we assessed if Na+/K+-ATPase also contributes to cutaneous thermal hyperemia induced by local skin heating, which is commonly employed to assess cutaneous endothelium-dependent vasodilation. Further, we assessed the extent to which NOS contributes to this response. Cutaneous vascular conductance (CVC) was measured continuously at four forearm skin sites in eleven young adults (4 women). After baseline measurement, local skin temperature was increased from 33 to 39 ºC to induce cutaneous thermal hyperemia. Once a plateau in CVC was achieved, each skin site was continuously perfused via intradermal microdialysis with either: 1) lactated Ringer s solution (control), 2) 6 mM ouabain, a Na+/K+-ATPase inhibitor, 3) 20 mM L-NAME, a NOS inhibitor, or 4) a combination of both. Relative the control site, CVC during the plateau phase of cutaneous thermal hyperemia (~50%max) was reduced by the lone inhibition of Na+/K+-ATPase (-19±8%max, P = 0.038) and NOS (-32±4%max, P < 0.001) as well as the combined inhibition of both (-37±9%max, P < 0.001). The magnitude of reduction was similar between NOS inhibition alone and combined inhibition (P = 1.000). The administration of Na+/K+-ATPase and NOS inhibitors fully abolished the plateau of CVC with values returning to pre-heating baseline values (P = 0.439). We show that Na+/K+-ATPase contributes to cutaneous thermal hyperemia during local skin heating to 39 ºC, and this response is partially mediated by NOS.