Fig. 6.

ET-1 receptor blockade does not alter the SMC hypoxia-induced proliferative, apoptotic, or migratory responses. A: in hPASMC, hypoxia (5% O₂) for 24 h increased proliferation. Inhibition of either the endothelin A or endothelin B (ETA or ETB) receptors had no effect on the proliferative response under normoxic conditions. Moreover, the hypoxia-induced increase in proliferation was not altered by pharmacological blockade of either the ETA receptor with BQ123 or the ETB receptor with BQ788. Cell proliferation was measured (n = 3; for each experimental condition) by BrdU incorporation assay after 24 h. **P < 0.01, hypoxia vs. normoxia. B: ET receptor blockade does not alter hPASMC apoptosis under both normoxic and hypoxic conditions. hPASMC apoptosis was measured after 24 h by CaspaseGlo assay to detect caspase 3/7 activities. Graph represents the means ± SE (n = 6; for each experimental condition) and is represented as a percentage of each respective control (control = 100%). C: ET receptor blockade does not alter hPASMC migration as assessed by modified Boyden Chamber assay. SMC were stimulated with or without 10 ng/ml PDGF-BB for 24 h. Graph represents the means ± SE of the number of SMC per HPF from 5 random fields per sample (n = 3; for each experimental condition). §§§P < 0.001, PDGF-BB vs. untreated.