eNOS and nNOS contribution to reflex cutaneous vasodilation during dynamic exercise in humans

Recent data suggests nNOS mediates NO‐component of reflex cutaneous vasodilation with passive heat stress. Our hypothesis was nNOS but not eNOS inhibition would attenuate reflex cutaneous vasodilation during dynamic exercise. Protocol 1: subjects performed a VO2 peak test on a supine cycle ergometer. Protocol 2: with experimental arm at heart level subjects cycled in supine posture at 60% VO2 peak to raise core temperature (Tc) 0.8–1.0°C (35–45 min). In protocol 2 subjects were equipped with 4 microdialysis fibers on the forearm and each randomly assigned as: 1) lactated Ringer's (control); 2) 5mM NPLA (nNOS inhibition); 3) 10mM L‐NIO (eNOS inhibition); and 4) 20mM L‐NAME (non‐selective NOS inhibition). At the end of protocol 2 all sites were locally heated to 43°C and infused with SNP to elicit maximal dilation. Mean arterial pressure (MAP), skin blood flow via laser‐Doppler flowmetry (LDF), and Tc via ingestible telemetric pill were measured; cutaneous vascular conductance (CVC) was calculated as LDF/MAP and normalized to maximum. In protocol 2 there was no significant difference between control (62±5 %CVCmax) and NPLA (61±6 %CVCmax). L‐NIO (38±4 %CVCmax) and L‐NAME (41±7 %CVCmax) significantly attenuated CVC compared to control and NPLA (p<0.001 all conditions). There was no difference between L‐NIO and L‐NAME. We conclude eNOS, not nNOS, contribute to reflex cutaneous vasodilation during dynamic exercise.