Our hypothesis was that KCa2.3 and KCa3.1 channels participate in maintaining endothelial function in the pulmonary vasculature, whereas deficiency of KCa2.3- and KCa3.1 channels aggravates endothelial dysfunction, and thereby contributes to pulmonary hypertension and the associated structural pathologies. The gene discussed is KCNN3; the disease is endothelial dysfunction.