Effect of Endoplasmic Reticulum Stress on Endothelial Ischemia-Reperfusion Injury in Humans.

Effect of Endoplasmic Reticulum Stress on Endothelial Ischemia-Reperfusion Injury in Humans. Am J Physiol Regul Integr Comp Physiol. 2020 Oct 14;: Authors: Hemingway HW, Moore AM, Olivencia-Yurvati AH, Romero SA Abstract Endoplasmic reticulum stress contributes to ischemia-reperfusion (I/R) injury in rodent and cell models. However, the contribution of endoplasmic reticulum stress in the pathogenesis of endothelial I/R injury in humans is unknown. We tested the hypothesis that compared with placebo, inhibition of endoplasmic reticulum stress via ingestion of tauroursodeoxycholic acid would prevent the attenuation of endothelium-dependent vasodilation following I/R injury. Twelve young adults (six women) were studied following ingestion of a placebo or 1,500 mg tauroursodeoxycholic acid (TUDCA). Endothelium-dependent vasodilation was assessed via brachial artery flow-mediated dilation (duplex ultrasonography) before and after I/R injury, which was induced by 20 min of arm ischemia followed by 20 min of reperfusion. Endothelium-independent vasodilation (glyceryl trinitrate-mediated vasodilation) was also assessed after I/R injury. Compared with placebo, TUDCA ingestion increased circulating plasma concentrations by 145 ± 90 ng ml-1 and increased concentrations of the taurine unconjugated form, ursodeoxycholic acid by 560 ± 156 ng ml-1 (both P < 0.01). Ischemia-reperfusion injury attenuated endothelium-dependent vasodilation, an ef...
Source: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology - Category: Physiology Authors: Tags: Am J Physiol Regul Integr Comp Physiol Source Type: research
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