Oxygen and vascular smooth muscle contraction

Abstract

Oxygen tension is an important determinant of the contractile tension developed by isolated helical strips of rabbit aorta. A decrease in PO2 [O2 pressure] below 100 mm Hg causes the contractile response to epinephrine (1-3 [mu]g/1) to diminish linearly to near 0 levels at < 1 mm Hg. If O2 tension is rapidly decreased from 100 mm Hg to a lower steady-state value during a sustained contraction produced by epinephrine, the time constant of decreased contractile tension is less than 4 min. If the smooth muscle is stimulated with epinephrine near the end of a 15-min hypoxic period, and contractile tension is allowed to reach a steady state, an increase in P02 to 100 mm Hg causes recovery of contractile tension, with a time constant of less than 2.5 min providing the PO2 during hypoxia is > 5 mm Hg. The time constant is approximately 3.5 min after 60 min of hypoxia (> 5 mm Hg). At 5 mm Hg or less, however, the time constant is 5.5 min after 15 min hypoxia, and is greater than 15 min after 60 min hypoxia. The immediate dependence of contractile tension on PO2 may be due to a metabolic role of O2 within the mitochondria of the smooth muscle cells, as the final electron acceptor in the respiratory chain. Such a rate-limiting metabolic device, which is rapidly reversible at PO2 between 5 and 130 mm Hg, could serve as a control for the production of high-energy intermediates necessary for vascular smooth muscle contraction and provide a means whereby PO2 could account for local autoregulation of blood flow in situ.