As mentioned previously, pulmonary arteries constrict in response to hypoxia and thereby regulate blood supply to the primary sites of gaseous exchange (81). Thus, HPV aids ventilation perfusion matching in the lung. In isolated pulmonary arteries, HPV is biphasic (Fig. 1A). Thus, hypoxia induces an initial transient constriction, which is then followed by a slow tonic constriction. It is apparent that HPV is a multifactorial process, with at least three discrete components of constriction (Fig. 1A) (22, 26). Our findings suggest that an initial transient (component 1) and maintained plateau (component 2) constriction are respectively promoted by direct effects of hypoxia on pulmonary artery smooth muscle (22, 23, 90). These components appear to be driven by two discrete mechanisms of Ca2+ release from the sarcoplasmic reticulum (SR). Full progression of HPV is then ensured by release of an endothelium-derived vasoconstrictor (component 3) (22, 26; see Chapters 6 and 12).
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