Negative Affective Responsivity to Daily Stressors and Microvascular Endothelial Function in Young-to-Middle Aged Adults

Heightened negative affective responsivity (NA-R) to daily stressors predicts increased cardiovascular disease (CVD)-related morbidity and mortality. Although greater daily stressor exposure has been linked to disrupted microvascular homeostasis, whether NA-R to daily stressors is associated with endothelial dysfunction remains unclear. Accordingly, the objective of this study was to test the hypothesis that greater NA-R to daily stressors would be related to reductions in microvascular endothelium-dependent dilation (EDD). Twenty-three young-to-middle aged adults (19 female; 18-53yrs) completed a daily mobile app-based interview for 8 consecutive days to assess daily stress processes and affective dynamics. On day 9, red cell flux (laser Doppler flowmetry) was measured in response to a standard local heating protocol (42°C) followed by intradermal microdialysis perfusion of N(G)-nitro-l-arginine methyl ester (L-NAME; 15mM) to quantify nitric oxide (NO)-dependent dilation. NA-R to daily stressors was operationalized as the intra-individual slope of the change in negative affect on stressor days compared to stressor-free days (multilevel modeling) and subsequently used to classify adults as either minimally-responsive or highly-responsive based on the lower and upper interquartile values (n=5/group), respectively. By design, NA-R to daily stressors was greater in highly-responsive adults [0.04±0.05 vs. 0.52±0.19; p<0.01], but there were no group differences in the frequency of exposure to daily stressors (minimally-responsive: 41±22% vs. highly-responsive: 51±17% of days; p=0.45). Local heating-induced EDD was blunted in highly-responsive adults (91±8 vs. 69±13% maximum vascular conductance; p=0.006), secondary to reductions in NO-dependent dilation (72±11 vs. 56±13%; p=0.038). These preliminary data suggest that amplified NA-R to daily stressors may be associated with microvascular endothelial dysfunction in young-to-midlife adults, potentially contributing to increased CVD risk. NIH P20GM113125 (PI Edwards) This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.