Both hypoxic endothelial cell conditioned medium and hypoxia elevate intracellular free calcium in pulmonary artery smooth muscle cells.

By using Ca(2+)-sensitive fluorescent probe, Fura- 2, the effects of endothelial cell-conditioned medium and hypoxia on intracellular free calcium ([Ca2+]i) in cultured pulmonary artery smooth muscle cell (PASMC) were studied. Normoxic porcine pulmonary artery endothelial cell-conditioned medium (NPAECCM) obviously elevated [Ca2+]i in PASMC, whereas the hypoxic porcine pulmonary artery endothelial cell conditioned medium (HPAECCM) significantly elevated [Ca2+]i in PASMC much more than NPAECCM. Both the effects of NPAECCM and HPAECCM were dependent on the cultured endothelial cell extracellular calcium concentrations, ranged from 1.8 mmol/L to 2.4 mmol/L. Meanwhile, hypoxia directly increased, which was partially inhibited by verapamil, [Ca2+]i in PASMC through Ca2+ influx pathway. The data suggest that the augmented regulation of endothelial cell on PASMC via Ca2+ second messenger system and the hypoxia-induced Ca2+ influx into PASMC, particularly the former, may be components of mechanisms underlying hypoxic pulmonary vasoconstriction and chronic pulmonary hypertension.