The main findings of the present study are that the deficits of the KCa2.3 and KCa3.1 channels failed to change hypoxia-induced pulmonary hypertension, and that chronic hypoxia up-regulated KCa2.3-gene expression (and also of KCa1.1) and increased NS309-induced relaxation in wild type mice. The gene discussed is KCNN4; the disease is pulmonary hypertension.