Journal of Applied Physiology, Vol 74, Issue 6 2896-2903, Copyright © 1993 by American Physiological Society

ARTICLES

Mechanisms of T-kinin-induced increases in macromolecule extravasation in vivo

X. P. Gao, W. G. Mayhan, J. M. Conlon, S. I. Rennard and I. Rubinstein
Department of Internal Medicine, University of Nebraska Medical Center, Omaha.

The purpose of this study was to investigate the mechanisms that mediate T-kinin- (Ile-Ser-bradykinin) induced increases in macromolecule extravasation in the hamster cheek pouch. Changes in plasma extravasation were quantified by counting the number of leaky sites and calculating the clearance of fluorescein isothiocyanate- (FITC) dextran (mol mass = 70 kDa) during suffusion of the cheek pouch with T-kinin (0.1-1.0 microM) by using intravital microscopy. T-kinin induced a significant time- and concentration-dependent increase in leaky site formation and clearance of FITC-dextran (P < 0.05). The increase in plasma extravasation in response to T-kinin was mediated by two mechanisms: a COOH-terminal-mediated stimulation of B2 bradykinin receptors in postcapillary venules and an NH2-terminal-mediated degranulation of mast cells leading to histamine release. Indomethacin and CP 96345, a selective nonpeptide neurokinin-1 receptor antagonist, had no significant effects on T-kinin-induced responses. We conclude that T-kinin increases macromolecule extravasation in the peripheral microcirculation by stimulating B2 bradykinin receptors in post-capillary venules and by degranulating mast cells.

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