Hypoxic pulmonary vasoconstriction (HPV)

Hypoxic pulmonary vasoconstriction (HPV), also referred to as the Euler-Liljestrand mechanism, is a physiological phenomenon in which small pulmonary arteries constrict in response to low alveolar oxygen tension. Its primary biological function is to divert blood flow from poorly ventilated areas of the lung to better-ventilated regions, thereby optimizing ventilation-perfusion matching and maximizing systemic oxygen delivery [1][2]. While essential for normal lung function, chronic or global HPV—such as that induced by high altitude or generalized lung disease—can lead to persistent increases in pulmonary vascular resistance and the development of pulmonary hypertension [3][4]. From a therapeutic perspective, HPV is not a single molecular target but a complex pathway involving oxygen-sensitive potassium channels (Kv), voltage-gated calcium channels, and Rho-kinase signaling within pulmonary artery smooth muscle cells [5]. Drugs like calcium channel blockers, phosphodiesterase-5 inhibitors, and endothelin receptor antagonists are frequently used to modulate this response in clinical settings to alleviate pulmonary hypertension or manage gas exchange [4][6].

Other names

Euler-Liljestrand mechanismHypoxic pulmonary responsePulmonary hypoxic vasoconstriction

Modulation of the pulmonary vascular tone through the inhibition of smooth muscle contraction or the promotion of vasodilation to counteract or enhance the physiological response to low oxygen levels.