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

X. P. Gao, W. G. Mayhan, J. M. Conlon, S. I. Rennard, I. Rubinstein

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17 Citations (Scopus)


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 μM) 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.

Original languageEnglish
Pages (from-to)2896-2903
Number of pages8
JournalJournal of Applied Physiology
Issue number6
Publication statusPublished - 1993
Externally publishedYes


  • compound 48/80
  • hamster
  • histamine
  • inflammation
  • mast cells
  • microcirculation
  • plasma extravasation
  • receptor antagonists

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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