Feline hypoxic pulmonary vasoconstriction is not blocked by the angiotensin I-converting enzyme inhibitor, captopril

R. L. Prewitt, Charles Leffler

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

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 The left lungs of 6 cats were pump-perfused through the left pulmonary artery with blood withdrawn from the inferior vena cava.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 F, 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 F 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.

Original languageEnglish (US)
Pages (from-to)293-298
Number of pages6
JournalJournal of Cardiovascular Pharmacology
Volume3
Issue number2
DOIs
StatePublished - Jan 1 1981

Fingerprint

Captopril
Felidae
Vasoconstriction
Angiotensin-Converting Enzyme Inhibitors
Angiotensin II
Lung
Angiotensin I
Dinoprost
Vascular Resistance
Respiration
Cats
Oxygen
Atrial Pressure
Inferior Vena Cava
Peptidyl-Dipeptidase A
Pulmonary Artery
Blood Vessels
Arterial Pressure
Gases

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

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abstract = "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 The left lungs of 6 cats were pump-perfused through the left pulmonary artery with blood withdrawn from the inferior vena cava.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 F2α, 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 F2α 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.",
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N2 - 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 F2α, 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 F2α 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.

AB - 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 F2α, 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 F2α 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.

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