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- W122367483 abstract "Chronic hypoxia (CH) influences Ca2+-dependent pulmonary arterial (PA) reactivity, and enhanced vasoreactivity is a risk factor in pulmonary disease. Using wire-myography, Western immunoblot, and Ca2+ imaging approaches of PA isolated from adult sheep housed under normoxic conditions or at 12,470 feet for ~ 110 days (CH), the hypothesis that CH alters Ca2+-dependent contractility was tested. Serotonin (5-HT; 10 μM) dependent PA contractility in CH was dependent on extracellular Ca2+, and 10 mM Ni2+ inhibited contractility and Ca2+ signaling. However, select Ca2+ entry pathways were altered by CH. CH reduced the role for L-type Ca2+ channels (CaL) as vasorelaxation to 10 μM nifedipine was blunted and α-subunit protein expression was reduced, although NIF reduced Ca2+ signals to control levels in CH. CH also reduced the role for non-selective cation channels (NSCC), as determined by serial application of 50 μM SKF 96365 to NIF treated arteries. Similarly, inhibition of reverse mode-Na+- Ca2+ exchange (NCX) with 10 μM KB-R7943 reduced contractility more dramatically in PA from normoxic sheep. Given extracellular Ca2+ removal and Ni2+ reduced contractility in CH while the roles for CaL, NSCC, and NCX were restricted, SKF-insensitive basal Ca2+ influx appears important to 5-HT-dependent contractility in PA from CH sheep. Support from NIH, NSF, UM, and LLUMC." @default.
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- W122367483 date "2009-04-01" @default.
- W122367483 modified "2023-09-27" @default.
- W122367483 title "Chronic hypoxia influences the role of extracellular Ca2+ influx during serotonin‐mediated contractility of pulmonary arteries from adult sheep" @default.
- W122367483 doi "https://doi.org/10.1096/fasebj.23.1_supplement.619.6" @default.
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