Abnormal endothelial function in the lungs plays a key role in pulmonary hypertension, with this study focusing on how different sizes of pulmonary arteries (PAs) contribute to this condition.
It was found that large proximal PAs predominantly rely on nitric oxide release for relaxation, while small distal PAs depend more on a process called endothelium-dependent hyperpolarization (EDH).
Chronic hypoxia disrupts EDH-mediated relaxation in small distal PAs by downregulating a protein called connexin 40 (Cx40), leading to increased pressure in the right ventricle, which is a significant factor in the development of pulmonary hypertension.