TRPV‐1 Channels Contribute to Cutaneous Active Vasodilation in Humans

Abstract

We tested the hypothesis that inhibition of TRPV-1 channels would attenuate cutaneous active vasodilation (AVD). Six subjects were equipped with four microdialysis fibers on the ventral forearm and each site was randomly assigned a drug treatment: 1) 90% propylene glycol + 10% lactated Ringer's (vehicle control); 2)10 mM L-NAME to inhibit NO synthase; 3) 20 mM capsazepine (CPZ) to inhibit TRPV-1 channels; 4) combined L-NAME + CPZ. Whole body heating (WBH) was achieved via water perfused suits to raise oral temperature 0.8°C above baseline. Systemic arterial pressure (SAP) was monitored and skin blood flow was measured via laser-Doppler flowmetry (LDF). Maximal skin blood flow was achieved by local heating to 43°C and infusion of 28mM nitroprusside. Cutaneous vascular conductance (CVC) was calculated as SAP/LDF and normalized to maximal. During WBH, CPZ sites were significantly reduced compared to CON sites (51±2% vs. 65±3% CVCmax, respectively; p < 0.05). L-NAME (32±1%CVCmax) sites were attenuated compared to CPZ. There was no difference between L-NAME and combined L-NAME + CPZ. These data suggest: 1)TRPV-1 receptors directly contribute to AVD; and 2) TRPV-1 channels account for a portion of the NO component.