Hypoxic Pulmonary Vasoconstriction in the Rat
The Necessary Role of Angiotensin II
In isolated blood-perfused rat lungs, brief periods of ventilation hypoxia (2% O2) produce pulmonary vasoconstriction. In isolated lungs perfused with a salt-albumin solution, hypoxia produces no pulmonary vasoconstrictor responses in most preparations and only minimal responses in others. Vasoactive agents including angiotensin II, phenylephrine, epinephrine, norepinephrine, bradykinin, histamine, serotonin, and methoxamine were added to the salt-albumin perfusate to determine which substance, if any, was necessary for a pulmonary vasoconstrictor response during hypoxia. The addition of angiotensin II (12-120 nM) to the perfusate during hypoxia resulted in marked pulmonary vasoconstriction in proportion to the amount of angiotensin II added (a maximal response to hypoxia occurred with 120 nM angiotensin II). None of the other agents had the same effect, nor was their vasoactivity dependent on angiotensin II. Angiotensin II augmented the hypoxic response in doses that are themselves subpressor; tachyphylaxis to the direct pressor activity of angiotensin II was not associated with attenuation of the hypoxic response. These results suggest that an action of angiotensin II that is separate from its pressor activity is specifically required for a significant vasoconstrictor response to hypoxia in isolated rat lungs.
- Received November 27, 1973.
- Accepted April 19, 1974.
- © 1974 American Heart Association, Inc.