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. 2022 Feb 24;42(4):428–443. doi: 10.1161/ATVBAHA.121.317365

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© 2022 The Authors.

Arteriosclerosis, Thrombosis, and Vascular Biology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 2. — Reduced contractile responses to various agonists and increased compliance of Y/T KO arteries. Tail arteries were mounted in a wire myograph and dose-response curves were generated by integrating force over 7 min for each dose of (A) AVP (vasopressin; Ctrl [control], n=7; Y/T KO, n=8), (B) 5-HT (serotonin; Ctrl, n=9; Y/T KO, n=9), (C) cirazoline, an α₁-adrenergic agonist (Ctrl, n=9; Y/T KO, n=9), and (D) U 46619, a thromboxane A2 analog (Ctrl, n=6; Y/T KO, n=6). E, Force development over 7-min stimulation with 60 mmol/L KCl (Ctrl, n=9; Y/T KO, n=9). F, The length-tension relationship of the abdominal aorta was determined in Ca²⁺-free HEPES-buffered solution (Ctrl, n=10; Y/T KO, n=8; Ctrl:vehicle-treated mice). All force measurements were normalized to the length of each preparation. All data are presented as mean±SEM. 5-HT indicates 5-hydroxytryptamine/ serotonin.