Ascorbic acid or L-arginine improves cutaneous microvascular function in chronic kidney disease

DuPont JJ, Farquhar WB, Townsend RR, Edwards DG. Ascorbic acid or L-arginine improves cutaneous microvascular function in chronic kidney disease. J Appl Physiol 111: 1561-1567, 2011. First published September 1, 2011; doi: 10.1152/japplphysiol.00419.2011.-We sought to determine whether oxidative stress or a relative deficit of L-arginine plays a role in reducing cutaneous vasodilation in response to local heating in chronic kidney disease (CKD). Eight patients with stage 3-4 CKD and eight age- and sex-matched healthy control (HC) subjects were instrumented with four microdialysis (MD) fibers for the local delivery of 1) Ringers solution (R), 2) 20 mM ascorbic acid (AA), 3) 10 mM L-arginine (L-Arg), and 4) 10 mM N-G-nitro-L-arginine methyl ester (L-NAME). Red blood cell (RBC) flux was measured via laser Doppler flowmetry. A standardized nonpainful local heating protocol (42 degrees C) was used. Cutaneous vascular conductance (CVC) was calculated as RBC flux/MAP and all data were expressed as a percentage of the maximum CVC at each site (28 mM sodium nitroprusside, T-loc = 43 degrees C). The plateau %CVCmax was attenuated in CKD (CKD: 76 +/- 4 vs. HC: 91 +/- 2%CVCmax; P < 0.05) and the NO contribution to the plateau was lower in CKD (CKD: 39 +/- 7, HC: 54 +/- 5; P < 0.05). The plateau %CVCmax in the CKD group was significantly greater at the AA and L-Arg sites compared with R (AA: 89 +/- 2; L-Arg: 90 +/- 1; R: 76 +/- 4; P < 0.05) and did not differ from HC. Initial peak %CVCmax was also significantly attenuated at the R and L-Arg sites in CKD (P < 0.05) but did not differ at the AA site. These results suggest that cutaneous microvascular function is impaired in stage 3-4 CKD and that oxidative stress and a deficit of L-arginine play a role in this impairment.