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Hypoxia activates Calcium‐dependent Chloride Channels in Small Pulmonary Artery Smooth Muscle Cells

In small pulmonary artery (SPA) smooth muscle cells (SMC), Cl−/HCO3− exchange seemed to set the level of intracellular pH (pHi) and inhibiting the exchanger prevented the pHi increase during hypoxia. We hypothesized that Ca2+ dependent Cl− channels (ClCa) channels played a role in acute hypoxic pulmonary vasoconstriction (HPV). In patch‐clamp studies using the cell‐attached‐patch configuration we recorded single ClCa channels at different patch potentials in cultured SMC from bovine SPA. Hypoxia increased ClCa channel open times, as did 20 μM caffeine. The ClCa 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 [Ca2+]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 ClCa currents and that they can be activated by hypoxia. Funding: Med Coll WI and VA Med Ctr.