3 years ago

Epithelial Na+ channel (ENaC) differentially contributes to shear stress-mediated vascular responsiveness in carotid and mesenteric arteries from mice.

Fiona J McDonald, Zoe Ashley, Martin Fronius, Sama Mugloo
A potential "new player" in arteries for mediating shear stress responses is the Epithelial Sodium Channel (ENaC). ENaC's contribution as shear sensor in intact arteries, and particularly different types of arteries (conduit and resistance) is unknown. We investigated the role of ENaC in both conduit (carotid) and resistance (3rd order mesenteric) arteries isolated from C57Bl/6J mice. Vessel characteristics were determined at baseline (60 mmHg, no-flow), in response to increased intraluminal pressure and shear stress using a pressure myograph. These protocols were performed in the absence and presence of the ENaC inhibitor amiloride (10 µM) and following inhibition of endothelial nitric oxide synthase (eNOS) by L-Name (100 µM). Under no-flow conditions, amiloride increased the internal and external diameter of carotid (13{plus minus}2%, p<0.05), but not mesenteric (0.5{plus minus}0.9%, p>0.05) arteries. In response to increased intraluminal pressure amiloride had no effect on the internal diameter of either type of artery. However, amiloride affected the stress/strain curves of mesenteric arteries. With increased shear stress ENaC-dependent effects were observed in both arteries. In carotid arteries, amiloride augmented flow-mediated dilation (9.2{plus minus}5.3%) compared with control (no amiloride, 6.2{plus minus}3.3%; p<0.05). In mesenteric arteries amiloride induced a flow-mediated constriction (-11.5{plus minus}6.6%) compared with control (-2.2{plus minus}4.5%; p<0.05). L-Name mimicked the effect of ENaC inhibition and prevented further amiloride effects in both types of arteries. These observations indicate that ENaC contributes to shear sensing in conduit and resistance arteries. The ENaC-mediated effects were associated with NO production although may involve different - artery dependent - downstream signalling pathways.

Publisher URL: http://doi.org/10.1152/ajpheart.00506.2017

DOI: 10.1152/ajpheart.00506.2017

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