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Salt‐Induced Hypertension Modulates Macrophage K + Channel Activity and Oxidative Burst Activity.
Author(s) -
ColdenStanfield Margaret
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1362-d
Subject(s) - respiratory burst , chemistry , oxidative phosphorylation , salt (chemistry) , macrophage , oxidative stress , medicine , biophysics , biochemistry , biology , in vitro
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.