OXYGEN SENSORS IN VASCULAR SMOOTH-MUSCLE

Inhibition or activation of cellular function due to acute decreases i n Po, can be considered in terms of two different processes: 1) a sens or that monitors PO2 decreases and 2) transduction systems directed fr om the O-2 sensor to reactions that control cellular function. We used the norepinephrine-contracted aortic smooth muscle model to study the nature of the O-2 sensor and transduction system during decreased PO2 -evoked relaxations. The phos phorylation potential, a measurement of kinetic energy required for ATP hydrolysis, was decreased to 30% of co ntrol at the onset of relaxation and progressively fell as muscle rela xed. The free inorganic phosphate intracellular concentration ([P-i]) was experimentally increased similar to 0.6 mM during transients that followed a rapid decrease in PO2. Relaxations to 80% of maximal force were more rapid under conditions of an augmented [P-i] than in control rings, and they occurred at a higher phosphocreatine concentration an d phosphocreatine-to-free creatine ratio but at the same phosphorylati on potential. Results support the operation of a cytochrome aa(3) O-2 sensor in the mechanism of decreased PO2-evoked relaxations and implic ate an increase in [P-i] and a decrease in kinetic energy in the trans duction mechanism directed at rate-limiting reactions that control for ce.