We measured acute vascular responses to heat stress to examine the hypothesis that macrovascular endothelial-dependent dilation is improved in a shear-dependent manner, which is further modified by skin temperature. Twelve healthy males performed whole-body heating (+1.5°C esophageal temperature), bilateral forearm heating (~38°C skin temperature), and a time-matched (~60 min) control condition on separate days in counterbalanced order. Bilateral assessments of blood flow and brachial artery flow-mediated dilation (FMD) were performed before and 10 min after each condition protocols with duplex Doppler ultrasound. To isolate the influence of shear stress, a pneumatic cuff was inflated (~90 mmHg) around the right forearm during each condition to attenuate heat-induced rises in blood flow and shear stress. After forearm heating, FMD increased [cuffed: 4.7 (2.9) to 6.8 (1.5)%, non-cuffed: 5.1 (2.8) to 6.4 (2.6)%] in both arms (time P<0.01). Whole-body heating also increased FMD in the non-cuffed arm from 3.6 (2.2) to 9.2 (3.2)% and in the cuffed arm from to 5.6 (3.0)% to 8.6 (4.9)% (time P<0.01). After the time control, FMD decreased [cuffed: 6.3 (2.4) to 4.7 (2.2)%, non-cuffed: 6.1 (3.0) to 4.5 (2.6)%] in both arms (time P=0.03). Multiple linear regression (adjusted r2=0.263, P=0.003) revealed that changes in esophageal temperature, skin temperatures, and heart rate explained the majority of the variance in this model (34%, 31% and 21%, respectively). Our findings indicate that, in addition to shear stress, skin and core temperatures are likely important contributors to passive heating-induced vascular adaptations.