Reflex Control of Cutaneous Vasoconstriction during Whole‐body Cooling in Aged Humans

Abstract

Reflex cutaneous vasoconstriction (VC) is impaired in human aging; however, the relative causative contributions of altered skin sympathetic nervous system activity (SSNA), signal transduction, and end‐organ responsiveness are unclear. We hypothesized that 1) whole‐body cold stress would elicit blunted SSNA responses in healthy older (O) compared to young (Y) adults and 2) cutaneous adrenergic responsiveness would be reduced in O adults. 10 Y (24±1 yrs) and 11 O adults (57±2 yrs) participated in two protocols. In Protocol 1, reflex VC was induced by gradual whole‐body cooling (mean skin temperature = 30.5°) using a water‐perfused suit. SSNA (peroneal microneurography) and red cell flux (laser Doppler flowmetry; dorsum of foot) were measured continuously. SSNA was expressed as a percentage of baseline. In Protocol 2, an intradermal microdialysis fiber was placed in the skin of the lateral calf to measure red cell flux in response to graded intradermal infusions of norepinephrine (NE; 10‐12 to 10‐2 M). In each study, cutaneous vascular conductance (CVC=flux/mean arterial pressure) was expressed as a change from baseline. Reflex cutaneous VC was attenuated in O adults (‐0.034±0.01 Y v. ‐0.018±0.01 O ΔCVCbase; P<0.05). SSNA increased during cooling in Y (273±37%; P<0.05) but not O adults (143±10%; P>0.05). There was no age‐related difference in cutaneous adrenergic responsiveness to exogenous NE (dose‐response logEC50; ‐6.6±0.4 Y vs. ‐7.0±0.3 O; P=0.57). These data demonstrate that age‐related impairments in reflex cutaneous VC are mediated in part by blunted SSNA responses and not by reduced cutaneous adrenergic responsiveness, suggesting that presynaptic synthesis and/or SSNA‐mediated release of vesicular NE is decreased in aged skin.