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- W184837448 abstract "K2P6.1, a Two-Pore Domain K channel expressed in vascular smooth muscle, is necessary to maintain normal peripheral vascular resistance and mean arterial pressure in C57/SV129 mice. However the functional state of the endothelium in these mice has not previously been assessed. We tested the hypothesis: K2P6.1- deficient mice (8–12 wks) have impaired endothelial-mediated relaxation due to elevation in endothelial-derived contracting factors. 24-hour mean telemetry of conscious mice showed elevated blood pressures (MAP 96±11 vs. 143±14 & SBP 109±12 vs. 158±11 mmHg in WT and KO mice respectively, n=6, p<0.05). Endothelial-mediated vasorelaxation of thoracic aorta was evaluated by isometric myography. Aorta were precontracted with phenylephrine (10-5M) and subsequently relaxed with carbachol (CCH) and acetylcholine (CCH). Relaxations were enhanced in KO aorta by 56±5% (n=9, p<0.001) and 33±5% (n=6, p<0.01) for CCH and ACH, respectively. In contrast, relaxations to ATP and ADP were impaired by 39±5% (n=8, p=0.01) and 38±6% (n=8, p<0.05) in KO aorta, but were normalized with 10-5M indomethacin (n=8). Indomethacin-sensitive contractions using non-precontracted aorta with 10-4M LNAME were elevated in KO mice to ACH by 66±2% (n=4, p=0.04) and to ATP by 41±4% (n=7, p=0.05). In summary, knockout of K2P6.1 either augments or inhibits vasorelaxation depending on the agonist system. Funded by NIH 5R21HL098921-02" @default.
- W184837448 created "2016-06-24" @default.
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- W184837448 date "2012-04-01" @default.
- W184837448 modified "2023-09-26" @default.
- W184837448 title "K2P6.1 Knockout Mice Have Varied Endothelial‐Mediated Relaxation With Elevated Endothelial‐Mediated Contraction" @default.
- W184837448 doi "https://doi.org/10.1096/fasebj.26.1_supplement.872.19" @default.
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