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ASIC1 Contributes to Store‐Operated Currents in Pulmonary Vascular Smooth Muscle

Store‐operated Ca2+ entry (SOCE) plays a significant role in pulmonary vasoregulatory mechanisms such as hypoxic pulmonary vasoconstriction and receptor‐mediated arterial constriction. Our laboratory has recently suggested that a unique family of non‐selective cation channels, the acid‐sensing ion channel 1 (ASIC1), contributes to SOCE in pulmonary arterial smooth muscle (PASM). To further investigate a role for ASIC1 in SOCE, we hypothesized that ASIC1 contributes to store‐operated Ca2+ currents in PASM cells. To test this hypothesis we measured cyclopiazonic acid (CPA)‐induced Ca2+ and Na+ currents using conventional whole cell patch‐clamp configuration in voltage‐clamp mode. We found that the ASIC inhibitors, amiloride (30 µM) and benzamil (10 µM), largely attenuated both CPA‐induced Ca2+ and Na+ currents in freshly isolated and primary cultured rat PASM cells. Consistent with these results, we additionally found that ASIC1 siRNA inhibited CPA‐induced Ca2+ and Na+ currents. In contrast, ASIC3 siRNA diminished CPA‐induced Na+ currents, but had no effect on Ca2+ currents, whereas ASIC2 siRNA was without effect on either CPA‐induced Ca2+ or Na+ currents. Together, these data provide further evidence for a novel role of ASIC1 in mediating SOCE in PASM. This work is supported by NIH and AHA.