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• W2979156968 endingPage "295" @default.
• W2979156968 startingPage "284" @default.
• W2979156968 abstract "<b><i>Background:</i></b> Arteries chronically constricted in culture remodel to smaller diameters. Conversely, elevated luminal shear stress (SS) promotes outward remodeling of arteries in vivo and prevents inward remodeling in culture in a nitric oxide synthase (NOS)-dependent manner. <b><i>Objectives:</i></b> To determine whether SS-induced prevention of inward remodeling in cultured arteries is specifically eNOS-dependent and requires dilation, and whether SS alters the expression of eNOS and other genes potentially involved in remodeling. <b><i>Methods:</i></b> Female mouse thoracodorsal arteries were cannulated, pressurized to 80 mm Hg, and cultured for 2 days with low SS (&#x3c;7 dyn/cm²), high SS (≥15 dyn/cm²), high SS + L-NAME (NOS inhibitor, 10^–4 M), or high SS in arteries from eNOS–/– mice. In separate arteries cultured 1 day with low or high SS, eNOS and connexin (Cx) 37, Cx40, and Cx43 mRNA were assessed with real-time PCR. <b><i>Results:</i></b> High SS caused little change in passive diameters after culture (–4.7 ± 2.0%), which was less than low SS (–18.9 ± 1.4%; <i>p</i> &#x3c; 0.0001), high SS eNOS–/– (–18.0 ± 1.5; <i>p</i> &#x3c; 0.001), or high SS + L-NAME (–12.0 ± 0.6%; nonsignificant) despite similar constriction during culture. Cx37 mRNA expression was increased (<i>p</i> &#x3c; 0.05) with high SS, but other gene levels were not different. <b><i>Conclusions:</i></b> eNOS is involved in SS-induced prevention of inward remodeling in cultured small arteries. This effect does not require NO-mediated dilation. SS increased Cx37." @default.
• W2979156968 created "2019-10-10" @default.
• W2979156968 creator A5002869032 @default.
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• W2979156968 date "2019-01-01" @default.
• W2979156968 modified "2023-09-23" @default.
• W2979156968 title "Shear Stress Attenuates Inward Remodeling in Cultured Mouse Thoracodorsal Arteries in an eNOS-Dependent, but Not Hemodynamic Manner, and Increases Cx37 Expression" @default.
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• W2979156968 doi "https://doi.org/10.1159/000502690" @default.
• W2979156968 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6908748" @default.
• W2979156968 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31574503" @default.
• W2979156968 hasPublicationYear "2019" @default.
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