Comparison of brachial dilatory responses to hypercapnia and reactive hyperemia

Flow-mediated dilation (FMD) relies on reactive hyperemia to stimulate the endothelium to release nitric oxide, causing smooth muscle relaxation. Hypercapnia also produces vasodilation, which is thought to be nitric oxide-independent. The purpose of this study was to compare and contrast the effects of hypercapnia and reactive hyperemia as stimuli for brachial artery dilation. On separate days, twenty-five participants underwent vasodilation studies via reactive hyperemia or hypercapnia (i.e. 10 mmHg increase in end-tidal carbon dioxide [PetCO2)]). During both studies changes in brachial artery diameter were recorded using continuous ultrasound imaging. Heart rate (HR) was measured throughout both tests. Resting HR (63  ±  11 versus 68  ±  14 beats min(-1), p  =  0.0027) and baseline brachial artery diameter measurements (4.57  ±  1.51 versus 5.28  ±  1.86 mm, p  =  0.022) were significantly different between reactive hyperemia and hypercapnia, respectively. HR at peak dilation (65  ±  11 versus 76  ±  14 beats min(-1), p  <  0.0001), peak vessel dilation (8.68  ±  4.50 versus 5.28  ±  1.86%, p  =  0.002), and time to peak dilation (90.8  ±  120.1 versus 658.3  ±  226.6 s, p  <  0.0001) were also significantly different between reactive hyperemia and hypercapnia. The dynamics by which reactive hyperemia and hypercapnia stimulate vasodilation appear to differ. Hypercapnia produces a smaller and slower vasodilatory effect than reactive hyperemia. Further research is necessary to better understand the mechanisms of vasodilation under hypercapnic conditions.