Shear-mediated dilation of the internal carotid artery is attenuated under hypocapnic conditions beyond reductions in shear stimulus.

Transient CO2 inhalation-induced dilation of the internal carotid artery (ICA), an index of cerebrovascular endothelial function, is partly mediated by cerebrovascular CO2 reactivity (CVR) via increased shear stress. Although CVR is attenuated under hypocapnia relative to normocapnia, it remains unclear whether the reduction in CVR affects ICA shear-mediated dilation. To address this knowledge gap, ICA shear-mediated dilation and ICA blood flow reactivity to CO2 ([Formula: see text]-CVR) were measured under normocapnia (Con) and hyperventilation-induced hypocapnia in 15 healthy adults (11M/4F, 25 ± 3 years) on two separate visits. Shear-mediated dilation was induced by elevating end-tidal CO2 partial pressure (PETCO2) by 10 mmHg above the pre-inhalation baseline for 30 s and calculated as the percentage increase in the peak diameter relative to the baseline diameter. The [Formula: see text]-CVR was assessed using a 3-min PETCO2 elevation (+ 10 mmHg) and expressed as the change in ICA blood flow divided by the change in PETCO2. Hypocapnia decreased [Formula: see text]-CVR (P = 0.02), shear-mediated dilation (4.12 ± 1.90% to 2.89 ± 1.44%, P = 0.02), and baseline diameter (P = 0.04) compared to normocapnia. Furthermore, reduced ICA dilation was associated with a decrease in the shear rate area under the curve above baseline (DSRAUC) (r(rm) = 0.59, P = 0.02). However, ICA dilation remained blunted after statistical adjustment for baseline diameter and DSRAUC (P = 0.02). Therefore, reduced CVR may partially attenuate ICA dilation through a reduced shear stimulus, while additional mechanisms, including increased cerebrovascular tone, may also contribute to blunted ICA dilation in hypocapnia.