Despite extensive investigations, we have yet to determine the precise mechanism by which hypoxia regulates cADPR accumulation. It seems likely that a change in the metabolic state of pulmonary artery smooth muscle will mediate this effect via one or a group of primary "metabolic sensor." In subsequent sections of this chapter, therefore, I will review the information currently available to us, in an effort to determine the likely identity of the "metabolic sensor(s)" and "metabolic effector(s)" involved.
When considering the possible mechanisms by which changes in cell metabolism may regulate cell activity, a logical place to start would be with a general consideration of the process of cellular 02 utilization and energy production (ATP) under normoxic conditions, with particular reference, as required, to arterial smooth muscle.
As we have all been informed from cradle to laboratory, there are two primary pathways to consider in this respect, namely glycolysis and oxidative phosphorylation by mitochondria, respectively. The activity of each pathway is inextricably linked, inversely with respect to anaerobic metabolism, due to homeostatic mechanisms that seek to maintain the desired cellular energy state.
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