Effect of t-kinin on microvascular permeability and its modulation
by peptidases in rat airways.
Yamawaki, Isao, Jun Tamaoki, Yuko Takeda, Atsushi Chiyotani, Noritaka
Sakai, Shinkichi Kameyama, Kimio Konno.
First Department of Medicine, Tokyo Women's Medical College, Tokyo
162, JAPAN
APStracts 2:0223A, 1995.
T-kinin (Ile-Ser-Bradykinin), the product of T-kininogen, has been
found in rat plasma during systemic inflammation, but the effect of
this kinin on airway inflammatory response is unknown. We examined
the effect of T-kinin on vascular permeability in airways of
anesthetized rats in vivo, using photometric measurement of the
extravasated Evans blue. Intravenous injection of T-kinin (0.1-10
[mu]mol/kg) increased dye extravasation in a dose-dependent manner,
with 134% for trachea and 117% for bronchi by 1 [mu]mol/kg.
Pretreatment with bradykinin B2 receptor antagonist, Hoe 140 (100
nmol/kg), but not the B1 receptor antagonist, des Arg9-Leu8
bradykinin (5 mg/kg), abolished plasma extravasation evoked by T
-kinin (1 [mu]mol/kg). NK1 tachykinin receptor antagonist, CP99,994 (4
mg/kg) did not affect T-kinin-induced vascular leakage. Pretreatment
with captopril (2.5 mg/kg), angiotensin converting enzyme (ACE)
inhibitor potentiated T-kinin (100 nmol/kg)-induced plasma
extravasation, whereas phosphoramidon (2.5 mg/kg), neutral
endopeptidase inhibitor had no effect. We conclude that T-kinin
produces airway vascular extravasation via stimulation of B2
receptors. The effect is modulated by endogenous ACE, and is not
mediated via activation of sensory nerve.
Received 30 December 1994; accepted in final form 16 May 1995.
APS Manuscript Number A1381-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.