Dual inhibition of angiotensin converting enzyme and neutral endopeptidase by omapatrilat in rat in vivo

2001 ◽  
Vol 44 (5) ◽  
pp. 411-418 ◽  
Author(s):  
Tom Bäcklund ◽  
Eeva Palojoki ◽  
Tina Grönholm ◽  
Anders Eriksson ◽  
Olli Vuolteenaho ◽  
...  
1994 ◽  
Vol 4 (22) ◽  
pp. 2715-2720 ◽  
Author(s):  
Stéphane De Lombaert ◽  
Jenny Tan ◽  
Lisa J. Stamford ◽  
Yumi Sakane ◽  
Carol Berry ◽  
...  

1994 ◽  
Vol 266 (2) ◽  
pp. L156-L162
Author(s):  
I. Yamawaki ◽  
P. Geppetti ◽  
C. Bertrand ◽  
B. Chan ◽  
J. A. Nadel

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.


Hypertension ◽  
1998 ◽  
Vol 32 (4) ◽  
pp. 778-785 ◽  
Author(s):  
Tuula Tikkanen ◽  
Ilkka Tikkanen ◽  
Melinda D. Rockell ◽  
Terri J. Allen ◽  
Colin I. Johnston ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document