Hypoxic pulmonary vasoconstriction (HPV) requires Ca²⁺ influx through store-operated Ca²⁺ channels (SOCC) in pulmonary arterial smooth muscle cells (PASMC) and is greater in distal than proximal pulmonary arteries (PA). SOCC may be composed of canonical transient receptor potential (TRPC) proteins and activated by stromal interacting molecule 1 (STIM1). To assess the possibility that HPV is greater in distal PA because store-operated Ca²⁺ entry (SOCE) is greater in distal PASMC, we measured intracellular Ca²⁺ concentration ([Ca²⁺]_i) and SOCE in primary cultures of PASMC using fluorescent microscopy and the Ca²⁺-sensitive dye, Fura-2. Increases in [Ca²⁺]_i due to hypoxia (4% O₂) but not KCl (60 mM) were greater in distal cells. In PASMC perfused with Ca²⁺-free solutions containing cyclopiazonic acid and nifedipine, the increase in [Ca²⁺]_i caused by restoration of extracellular Ca²⁺ and the decrease in Fura-2 fluorescence caused by Mn²⁺ were greater in distal PASMC, indicating greater SOCE. The increased SOCE caused by hypoxia was also greater in distal cells. Real-time quantitative polymerase chain reaction (qPCR) analysis of PASMC and freshly isolated de-endothelialized PA tissue demonstrated expression of STIM1 and five of seven known TRPC isoforms (TRPC1>TRPC6>TRPC4>>TRPC3TRPC5). For both protein, as measured by Western blotting, and mRNA, expression of STIM1, TRPC1, TRPC6, and TRPC4 was greater in distal than proximal PASMC and PA. These results provide further support for the importance of SOCE in HPV, and suggest that HPV is greater in distal than proximal pulmonary arteries because greater numbers and activation of SOCC in distal PASMC generate bigger increases in [Ca²⁺]_i.