Effect of severe hypoxia on the pulmonary vascular response to vasoconstrictor agents

When isolated blood-perfused pig lungs are exposed to inspired O2 tensions (PIO2) below 30 Torr, hypoxic pulmonary vasoconstriction is transient. To determine whether this transience is caused by a decrease in the amount of ATP available for maintenance of smooth muscle contraction, we compared normoxic (PIO2 = 100 Torr) and hypoxic (PIO2 = 10 Torr) dose-response curves to infusions of prostaglandin F2 alpha (PGF2 alpha), angiotensin II (AII), and potassium chloride (KCl). Hypoxia caused reversible depression of the responses to PGF2 alpha and AII but had no effect on the response to KCl. Because during hypoxia the lung was capable of an undiminished vasoconstrictor response to at least one agent, it seems unlikely that the supply of ATP available for contraction was limiting. The mechanism for the transience of the vasoconstrictor response to low PO2 values and the depression of the response to AII and PGF2 alpha remains unknown, but could involve depression of ATP production sufficient to limit some energy-requiring process other than contraction or release of a vasodilator.