Feline hypoxic pulmonary vasoconstriction is not blocked by the angiotensin I-converting enzyme inhibitor, captopril.
Because of evidence that angiotensin II may be necessary for pulmonary hypoxic vasoconstriction, we investigated the response to 3% oxygen breathing before and after the blockade of angiotensin I-converting enzyme with captopril. The left lungs of 6 cats were pump-perfused through the left pulmonary artery with blood withdrawn from the inferior vena cava. The animals were ventilated mechanically, and blood gases and pH were measured and maintained within normal limits. The pulmonary vascular resistance was calculated from measurements of pulmonary arterial pressure, left atrial pressure, and blood flow. Changes in pulmonary vascular resistance caused by 3% oxygen breathing, prostaglandin F2 alpha, angiotensin I, and angiotensin II were measured before and after captopril (20 mg/kg, i.v.). The pulmonary vascular response to hypoxia was not altered by the blockade of angiotensin II production. The responses to prostaglandin F2 alpha, and angiotensin II were unchanged as well, indicating that the vasoactivity of the pulmonary vessels was not altered. The response to angiotensin I was eliminated completely. These results indicate that angiotensin II is not necessary for, and does not alter, hypoxic pulmonary vasoconstriction in the cat.
D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D002415:Cats; D000860:Hypoxia / Q000503:physiopathology*; D011392:Proline / Q000031:analogs & derivatives*; D011652:Pulmonary Circulation / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D011392:Proline; D002216:Captopril