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• W3176787714 abstract "Acid-sensing ion channels (ASICs) are widely expressed cation channels of the ENaC/Degenerin superfamily which conduct hyperpolarizing inward cation currents through the plasma membrane in response to a variety of stimuli. Our laboratory previously defined the role of ASIC1 as a mediator of chronic hypoxia (CH) –induced pulmonary hypertension. ASIC2 and ASIC3 are also expressed in pulmonary arteries, but their roles in the regulation of pulmonary vascular resistance and the development of CH-induced pulmonary hypertension have not been investigated. ASIC2 and ASIC3 primarily conduct Na+ and therefore may play a role in the regulation of membrane potential in pulmonary artery smooth muscle cells (PASMC). We hypothesized that these channels contribute to pulmonary vasoreactivity and the development of CH-induced pulmonary hypertension. Interestingly, we found that acute hypoxia-, U46619-, and high KCl-induced increases in pulmonary vascular resistance were augmented in isolated-perfused lungs from ASIC2 knockout (ASIC2−/−) and ASIC3 knockout (ASIC3−/−) mice compared to wild-type (WT) mice, indicating that both ASIC2 and ASIC3 play inhibitory roles in these responses. Since increased acute pulmonary vasoreactivity could be associated with an exaggerated hypertensive response to CH-exposure we also tested the role of ASIC2 and ASIC3 in the development of CH-induced pulmonary hypertension. Right ventricular systolic pressure (RVSP), measured under isoflurane anesthesia, was not different between normoxia-exposed ASIC2−/− or ASIC3−/− and WT mice. Following 4 weeks of CH exposure (PB = 0.5 atm), RVSP was higher in CH− exposed ASIC2−/− compared to CH-exposed WT and ASIC3−/− mice. These data indicate that although ASIC2 and ASIC3 both play inhibitory roles in acute pulmonary vasoreactivity, only ASIC2 plays an inhibitory role in the development of CH-induced pulmonary hypertension. ASICs have been implicated in central chemoreception and ventilatory responses to hypercapnia and hypoxia raising the possibility that ASIC2−/− mice develop more severe hypoxemia than WT mice during exposure to hypoxia, so we measured arterial blood gases in both normoxia- and CH-exposed WT and ASIC2−/− mice in room air and during exposure to hypoxia or hypercapnia. Arterial O2, CO2, and pH levels were not different between WT and ASIC2−/− mice under any of these conditions, indicating that the exaggerated hypertensive response of ASIC2−/− mice to CH is not a result of more severe hypoxemia. In conclusion, ASIC2 and ASIC3 both play inhibitory roles in hypoxia-, U46619-, and KCl-induced pulmonary vasoconstriction, and ASIC2 protects against CH-induced pulmonary hypertension. Future studies will address the mechanisms of these roles, investigating the possibilities that ASIC2 and ASIC3 inhibit the activity of ASIC1 in PASMC, or that ASIC2 and ASIC3 reside in endothelial cells, contributing to endothelial inhibition of pulmonary vasoconstriction. Support or Funding Information Supported by National Heart, Lung, and Blood Institute Grants R01 HL-111084 (to N.L. Jernigan), T32 HL007736 (to T.C. Resta), National Institute of General Medical Science R25 GM060201 (to M.C. Werner-Washburne), and K12 (to A. Wandinger-Ness) This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal." @default.
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• W3176787714 date "2018-04-01" @default.
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• W3176787714 title "Acid‐Sensing Ion Channels (ASICs) 2 and 3 Buffer Pulmonary Vasoreactivity and ASIC2 Protects Against the Development of Chronic Hypoxia ‐Induced Pulmonary Hypertension" @default.
• W3176787714 doi "https://doi.org/10.1096/fasebj.2018.32.1_supplement.892.1" @default.
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