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- W156696118 abstract "Previous work on isolated perfused proximal tubules (PTs) shows that: (1) raising basolateral (BL) [CO2] markedly increases HCO3 reabsorption rate (JHCO3) and (2) blocking apical AT1 receptors or knocking out AT1A receptors eliminates the JHCO3 response to [CO2]BL. We hypothesize that the “orphaned” RPTPγ, with an extracellular carbonic-anhydrase-like domain, is a CO2 sensor. We perfused PTs from wild-type vs RPTPγ-null mice, using out-of-equilibrium solutions to vary [CO2]BL at fixed [HCO3]BL and pHBL. In wild-type PTs, raising [CO2]BL from 0% to 5% (“baseline”) to 20% (fixed [HCO3]BL = 22 mM, pHBL = 7.4) increased JHCO3 from 79 ± 6 (n = 14) to 136 ± 7 (n = 40) to 189 ± 4 pmol mm−1 min−1 (“pmm”, n = 14). In RPTPγ-null PTs, baseline JHCO3 was reduced by 23% to 105 ± 7 pmm (n = 24, p = 0.002, 1-way ANOVA), and the responses to 0% [CO2]BL (JHCO3 = 98 ± 7, n = 6) and 20% [CO2]BL (JHCO3 = 105 ± 12, n = 6) were eliminated. Finally, when we added 10−8 M candesartan (non-peptide AT1 antagonist) to the lumen of RPTPγ-null PTs, baseline JHCO3 was further fell by 29% to the “pedestal” level (JHCO3 = 75 ± 8 pmm, n = 18, p = 0.012, 1-way ANOVA). Moreover, and the responses to 0% [CO2]BL (JHCO3 = 58 ± 8, n = 4) and 20% [CO2]BL (JHCO3 = 83 ± 23, n = 5) were eliminated. Thus, knocking out RPTPγ eliminates the PT response to changes in [CO2]BL, consistent with the idea that RPTPγ is a CO2 sensor, as part of a signal-transduction cascade that also requires the apical AT1 receptor." @default.
- W156696118 created "2016-06-24" @default.
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- W156696118 date "2010-04-01" @default.
- W156696118 modified "2023-09-27" @default.
- W156696118 title "Effect of knocking out receptor protein tyrosine phosphatase γ (RPTPγ) in the CO 2 ‐induced stimulation of HCO 3 reabsorption by mouse renal proximal tubules" @default.
- W156696118 doi "https://doi.org/10.1096/fasebj.24.1_supplement.1024.7" @default.
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