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Hypoxia activates Calcium‐dependent Chloride Channels in Small Pulmonary Artery Smooth Muscle Cells
Author(s) -
Elsen Frank P,
Madden Jane A
Publication year - 2008
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.22.1_supplement.1174.7
Subject(s) - niflumic acid , hypoxic pulmonary vasoconstriction , chemistry , patch clamp , chloride channel , biophysics , hypoxia (environmental) , pulmonary artery , calcium , medicine , oxygen , biochemistry , biology , receptor , organic chemistry
In small pulmonary artery (SPA) smooth muscle cells (SMC), Cl − /HCO 3 − exchange seemed to set the level of intracellular pH (pH i ) and inhibiting the exchanger prevented the pH i increase during hypoxia. We hypothesized that Ca 2+ dependent Cl − channels (Cl Ca ) channels played a role in acute hypoxic pulmonary vasoconstriction (HPV). In patch‐clamp studies using the cell‐attached‐patch configuration we recorded single Cl Ca channels at different patch potentials in cultured SMC from bovine SPA. Hypoxia increased Cl Ca channel open times, as did 20 μM caffeine. The Cl Ca channel antagonist, niflumic acid (100 μM) reduced open times. Using the whole‐cell patch‐clamp configuration we recorded Cl − current amplitudes evoked with a given [Ca 2+ ]i at different test potentials. We determined Cl − as the conducting ion species by comparing the set Cl − equilibrium potential (20 mV) with measured results (∼22 mV). These single channel and whole‐cell current studies show that SPA SMC possess Cl Ca currents and that they can be activated by hypoxia. Funding: Med Coll WI and VA Med Ctr.