Endothelial Function Following IV Ascorbic Acid in Young Adults Who Habitually Consume a High Sodium Diet
Authors: Patik Jordan , Schade Serena , Lincoln Zoe , Mehrer Justin , Sanroman-Espinosa Diana , Lennon Shannon , Farquhar William , Edwards David 
Published: May 2023

Introduction: Despite recommendations to ingest <2.3 g of sodium/day, Americans consume an average of 3.4 g daily. The mechanisms through which this excess sodium intake may contribute to cardiovascular disease risk are not fully understood. We have demonstrated that a 7-day high sodium diet containing ~7 g/day blunts endothelium-dependent dilation in normotensive, salt resistant individuals. Ample evidence suggests that oxidative stress contributes to the vascular consequences of experimental high sodium diets. However, it is unknown whether chronic consumption of dietary sodium typical of the average American results in oxidative stress-induced reductions in endothelium-dependent dilation. Therefore, we tested the hypothesis that an acute systemic infusion of the antioxidant ascorbic acid (AA) would augment brachial artery flow-mediated dilation (FMD) in normotensive, non-obese young adults who habitually consume ≥3.4 g/day of dietary sodium. Methods: Twenty-nine participants (13M/16F, 28±6 y) were included based on a 3-day diet record screening. After at least 15 min of supine rest, brachial artery diameter and blood velocity were recorded via duplex ultrasound before and for 3 min after a 5-min occlusion of the forearm. A 20-min infusion of 0.06 g of AA/kg fat free mass dissolved in 100 ml normal saline was administered intravenously at a rate of 5 ml/min. Subsequently, a maintenance AA dose of 0.02 g/kg fat free mass was then infused at 2 ml/min while testing was repeated. All recordings were analyzed via edge tracking software with FMD calculated as the peak diameter change relative to baseline diameter and brachial artery shear rate calculated as 4✕velocity/diameter. Results: Habitual sodium intakes at screening averaged 4.5±1.1 g/day while urinary sodium excretion the day prior to the study visit was 136±57 mmol/24 hr. Following AA, time-to-peak dilation of the brachial artery was reduced from 51±14 to 42±9 s (P<0.001). Likewise, shear rate area under the curve (AUC) to peak dilation was also reduced after AA (3.3±1.5 x104 vs. 2.7±1.5 x104 a.u., P=0.001). FMD was unchanged from pre-AA to post-AA (8.6±3.0 vs. 8.0±3.6%, P=0.26). FMD remained similar after covarying for shear AUC (P=0.60). In contrast, indices of microvascular reactivity were reduced from pre-AA to post-AA, including post-occlusion peak blood flow (Δ-48.7±65.7 ml/min, P<0.001) and total reactive hyperemia (Δ-37.4±46.9 ml, P<0.001). Conclusions: These preliminary data indicate that acute systemic antioxidant treatment does not augment brachial artery endothelium-dependent dilation in normotensive, non-obese young adults who consume or exceed the national average daily sodium intake. This finding suggests that oxidative stress does not reduce conduit artery endothelial function in this population. Further investigation is needed to understand our observation of a diminished post-occlusion microvascular response after AA. This work was supported by the National Institutes of Health (5R01HL104106 and 5P20GM113125) and the American Heart Association (20POST35080171). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.