Aims: Hypoxic pulmonary vasoconstriction (HPV) is a physiological response to alveolar hypoxia that diverts blood flow from poorly ventilated to better aerated lung areas to optimize ventilation-perfusion matching. Yet, the exact sensory and signalling mechanisms by which hypoxia triggers pulmonary vasoconstriction remain incompletely understood. Recently, ATP release via pannexin 1 (Panx1) and subsequent signalling via purinergic P2Y receptors has been identified as regulator of vasoconstriction in systemic arterioles.
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
June 2020
Hypoxic pulmonary vasoconstriction (HPV) in combination with hypercapnic pulmonary vasoconstriction redistributes pulmonary blood flow from poorly aerated to better ventilated lung regions by an active process of local vasoconstriction. Impairment of HPV results in ventilation-perfusion mismatch and is commonly associated with various lung diseases including pneumonia, sepsis, or cystic fibrosis. Although several regulatory pathways have been identified, considerable knowledge gaps persist, and a unifying concept of the signaling pathways that underlie HPV and their impairment in lung diseases has not yet emerged.
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