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- W66566473 abstract "Macrophage infiltration contributes to end-organ kidney damage in salt-induced hypertension. We compared whole-cell ionic currents from bone marrow-derived macrophages (BMDMs) isolated from Dahl salt-resistant (SR) or salt-sensitive (SS) rats on a high-salt diet for 2 or 4 wk. After 2 wk, 75% of SR BMDMs possessed a large depolarization-evoked delayed outward rectifier K+ (Kdr) current. In 25% of the cells, an inward rectifier K+ (Kir) current was evoked during hyperpolarization. Resting membrane potential (RMP) in SR BMDMs was −39 mV. In contrast, 56% of SS BMDMs after 2 wk possessed Kir currents and smaller Kdr currents hyperpolarizing the membrane to −46 mV. There was no change in Kir currents in SR or SS BMDMs after 4 wk. However, Kdr currents were further reduced in both 4-wk SR and SS BMDMs compared to 2-wk BMDMs. RMP was −55 mV in 4-wk SS BMDMs. While basal oxidative burst activity was not different after 2 wk in SR or SS BMDMs, there was a 30% increase in basal activity in SS BMDMs after 4 wk compared to a 10% increase in SR BMDMs. Only SS BMDMs responded to an acute exposure to PMA with a 24% or 84% augmentation of oxidative burst activity after 2 or 4 wk, respectively. The modulation of macrophage cellular function including K+ channel activity by a high-salt environment may be important in the pathogenesis of kidney end-organ damage in salt-induced hypertension. This research was supported by NHLBI/K01HL076628-03." @default.
- W66566473 created "2016-06-24" @default.
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- W66566473 date "2007-01-01" @default.
- W66566473 modified "2023-09-23" @default.
- W66566473 title "Salt‐Induced Hypertension Modulates Macrophage K + Channel Activity and Oxidative Burst Activity." @default.
- W66566473 doi "https://doi.org/10.1096/fasebj.21.6.a1362-d" @default.
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