[T-kinin-induced increase in airway vascular permeability and its modulation by angiotensin-converting enzyme].
We studied the effect of T-kinin on airway vascular permeability and its modulation by endogenous peptidases in anesthetized rats in vivo, Vascular permeability was assessed by photometric measurement of extravasated Evans blue dye after formamide extraction. Intravenous injection of T-kinin increased dye extravasation in the trachea and main bronchi in a dose-dependent manner. Plasma extravasation evoked by T-kinin was inhibited by Hoe 140, a B2 receptor but-not by des Arg9-Leu8-bradykinin, a B1 receptor antagonist. Treatment with captopril, an angiotensin-converting enzyme inhibitor, potentiated the T-kinin-induced plasma extravasation, whereas phosphoramidon, a neutral endopeptidase inhibitor, had no effect. These results suggest that T-kinin increases airway vascular permeability via stimulation of B2 receptors, and that this effect is modulated by endogenous angiotensin-converting enzyme.
Takeda
Y
Y
First Department of Medicine, Tokyo Women's Medical College, Japan.
Tamaoki
J
J
Yamawaki
I
I
Chiyotani
A
A
Konno
K
K
D000818:Animals; D001920:Bradykinin / Q000031:analogs & derivatives* / Q000494:pharmacology; D001980:Bronchi / Q000187:drug effects* / Q000378:metabolism; D002199:Capillary Permeability / Q000187:drug effects*; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014132:Trachea / Q000187:drug effects* / Q000378:metabolism
C039065:T-kinin; D007703:Peptidyl-Dipeptidase A; D001920:Bradykinin