Oxygen and vascular smooth muscle contraction.

DETAR, REED, AND DAVID F. BOHR. Oxygen and vascular smooth muscle contraction. Am. J. Physiol. 214(Z): 241-244. 1968.-Oxygen tension is an important determinant of the contractile tension developed by isolated helical strips of rabbit aorta. A decrease in PO:! below 100 mm Hg causes the contractile response to epinephrine (l-3 pg/liter) to diminish linearly to near zero levels at < 1 mm Hg. If oxygen 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 PO? to 100 mm Hg causes recovery of contractile tension, with a time constant of less than 2.5 min providing the PO:! 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 hypoxiaThe immediate dependence of contractile tension on PO? is explained on the assumption that oxygen plays a metabolic role 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 Paz between 5 and 100 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 PO:! could account for local autoregulation of blood flow in situ.