AJP - Lung Cellular and Molecular Physiology, Vol 266, Issue 2 156-L162, Copyright © 1994 by American Physiological Society
Airway vasodilation by bradykinin is mediated via B2 receptors and modulated by peptidase inhibitors
I. Yamawaki, P. Geppetti, C. Bertrand, B. Chan and J. A. Nadel
Cardiovascular Research Institute, University of California, San Francisco 94143-0130.
We studied the effect of exogenous bradykinin on blood flow in the airway
microcirculation of anesthetized F344 rats in vivo. We made three
successive determinations of airway blood flow and cardiac output using a
modification of the reference sample microsphere technique. Injection of
bradykinin into the left ventricle increased airway blood flow in a
dose-related manner. Pretreatment with the bradykinin B2 receptor
antagonist, Hoe 140, completely abolished bradykinin-, but not
histamine-induced vasodilation. A bradykinin B1 receptor agonist,
[des-Arg9]bradykinin, did not affect airway blood flow. We also studied the
effect of inhibitors of angiotensin-converting enzyme (captopril) and
neutral endopeptidase (phosphoramidon) on bradykinin-induced vasodilation.
Pretreatment with captopril, but not phosphoramidon, potentiated the
bradykinin-induced vasodilation. However, the addition of phosphoramidon
further potentiated the effect of captopril. We conclude that injection of
bradykinin into the left ventricle produces a dose-related vasodilation in
the airway microcirculation mediated via B2 receptors, an effect that is
modulated primarily by angiotensin-converting enzyme and, to a lesser
extent, by neutral endopeptidase.
