Acute exposure to hypoxia increases pulmonary arterial pressure in rats (Fig. 4A) and causes a sustained yet reversible contraction of both isolated pulmonary arteries (Fig. 4B) and isolated PASMC (59, 117, 120). Functional removal of endothelium enhances HPV in isolated PA rings (120), suggesting that HPV is intrinsic to the individual PASMC independent of the endothelium, neuronal control, and circulating regulators. All of the machinery required to sense and respond to hypoxia and regulate pulmonary vascular tone is integrated within the individual PASMC (45, 46, 59, 120). HPV depends on external Ca2+ and is caused by a rise in [Ca2+]cyt due, partially, to membrane depolarization-mediated opening of VDCC. This is supported by studies showing that the hypoxic contractile response is almost abolished by removal of extracellular Ca2+ (Fig. 4B) and the hypoxic pressor effect in intact rats and isolated perfused lungs is blunted by the VDCC blockers, verapamil and nifedipine (Fig. 4A) (52). In addition to opening VDCC, recent studies suggest that acute hypoxia could also raise [Ca2+]cytvia capacitative Ca2+entry (CCE) or, possibly, voltage-independent pathways (see Chapters 6 and 9) (89). HPV is a critical physiological process for maximal oxygenation of venous (or pulmonary arterial) blood, therefore, it must be assured by multiple redundant mechanisms or pathways.
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