Acute exposure to oscillatory shear stress impairs endothelial function in oral contraceptive pill users across pill phases.

Abstract

Acute exposure to oscillatory shear stress (OSS), characterized by low mean and high retrograde shear stress, can impair endothelial function in humans. However, the majority of studies have only included men and none have assessed the impact of oral contraceptive pills (OCPs) on OSS-induced endothelial function impairment. Oxidative stress is higher in OCP users versus nonusers with the highest oxidative stress in the active pill (AP; synthetic hormone) compared to the placebo pill (PP; no synthetic hormone) phase. As oxidative stress is a key mechanism linking OSS and impaired endothelial function, we hypothesized that OCP users would experience OSS-induced impairment in endothelial function in both phases with the greatest decline occurring in the AP phase. Flow-mediated dilation (FMD; via Duplex ultrasound) was assessed before and after an OSS (30-min 70-mmHg cuff occlusion) and control condition (30-min rest) in 27 OCP users (20 ± 1 years) during the AP and PP phase of the OCP cycle. A condition × time interaction (P < 0.001) was detected with lower percent FMD post-OSS (Pre = 5.8 ± 2.3%; Post = 4.2 ± 2.3%) but not postcontrol (Pre = 5.3 ± 2.3%; Post = 5.4 ± 2.3%). The impact of OSS on %FMD did not differ between the AP and PP phase (phase × condition × time: P = 0.881). In conclusion, OCP users demonstrated a decline in FMD following acute exposure to OSS, which was not impacted by the phase of the OCP cycle. Future research should explore whether endothelial function responses to OSS vary across different hormonal statuses and types of contraceptive use.NEW & NOTEWORTHY Oscillatory shear stress is a proatherogenic blood flow pattern characterized by low mean and high retrograde flow. Endothelial function is impaired following exposure to oscillatory shear stress in men. This article provides the first evidence that oral contraceptive pill users experience an impairment in flow-mediated dilation following an acute exposure to oscillatory shear stress that does not differ across OCP phases.