Metabolic Regulation of cADPR Accumulation

Our findings and those of others offer two possible mechanism by which hypoxia may regulate cADPR synthesis and thereby promote HPV. Our findings suggest that an increase in cADPR levels by hypoxia may be mediated, in part, by an increase in levels, which has been shown to occur in pulmonary artery smooth muscle (59). Alternatively, cADPR synthesis could be increased as a result of superoxide generation by mitochondria (34), or by a previously unidentified mechanism (see Chapter 18).

Figure 4. A Po2 window for HPV in isolated arteries. A: Maintained constriction by hypoxia increases in magnitude between 50 and 60 Torr, but fails under near anoxic conditions (5-8 Torr). In contrast, the transient phase 1 constriction increases in magnitude progressively between 50 and 5 Torr. B: cADPR levels in pulmonary artery smooth muscle from 3rd order branches of the pulmonary artery tree under normoxic (20% 02), hypoxic (2% 02), and near anoxic (0% 02, 5-8 Torr) conditions, respectively. C: Effect of step-wise changes in 02 supply on a pulmonary artery ring without endothelium, after induction of maintained HPV with 2% 02 (16-21 Torr).

Figure 4. A Po2 window for HPV in isolated arteries. A: Maintained constriction by hypoxia increases in magnitude between 50 and 60 Torr, but fails under near anoxic conditions (5-8 Torr). In contrast, the transient phase 1 constriction increases in magnitude progressively between 50 and 5 Torr. B: cADPR levels in pulmonary artery smooth muscle from 3rd order branches of the pulmonary artery tree under normoxic (20% 02), hypoxic (2% 02), and near anoxic (0% 02, 5-8 Torr) conditions, respectively. C: Effect of step-wise changes in 02 supply on a pulmonary artery ring without endothelium, after induction of maintained HPV with 2% 02 (16-21 Torr).

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