Role of cyclooxygenase in the vascular response to locally delivered acetylcholine in Caucasian and African descent individuals

Abstract

This is an accepted manuscript of an article published by Elsevier in Microvascular Research on 17/01/2017, available online: https://doi.org/10.1016/j.mvr.2017.01.005 The accepted version of the publication may differ from the final published version.© 2017 Elsevier Inc. Introduction Individuals of African descent (AFD) are more susceptible to non-freezing cold injury (NFCI) compared with Caucasian individuals (CAU). Vasodilatation to acetylcholine (ACh) is lower in AFD compared with CAU in the non-glabrous foot and finger skin sites; the reason for this is unknown. Prostanoids are responsible, in part, for the vasodilator response to ACh, however it is not known whether the contribution differs between ethnicities. Methods 12 CAU and 12 AFD males received iontophoresis of ACh (1 w/v%) on non-glabrous foot and finger skin sites following placebo and then aspirin (600 mg, single blinded). Aspirin was utilised to inhibit prostanoid production by inhibiting the cyclooxygenase (COX) enzyme. Laser Doppler flowmetry was utilised to measure changes in skin blood flow. Results Not all participants could receive iontophoresis charge due to high skin resistance; these participants were therefore excluded from the analyses. Foot: ACh elicited greater maximal vasodilatation in CAU than AFD following placebo (P = 0.003) and COX inhibition (COXib) (P < 0.001). COXib did not affect blood flow responses in AFD, but caused a reduction in the area under the curve for CAU (P = 0.031). Finger: ACh elicited a greater maximal vasodilatation in CAU than AFD following placebo (P = 0.013) and COXib (P = 0.001). COXib tended to reduce the area under the curve in AFD (P = 0.053), but did not affect CAU. Conclusions CAU have a greater endothelial reactivity than AFD in both foot and finger skin sites irrespective of COXib. It is concluded that the lower ACh-induced vasodilatation in AFD is not due to a compromised COX pathway.Published versio