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

X. P. Gao, William Mayhan, J. M. Conlon, Stephen Israel Rennard, I. Rubinstein

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

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 (US)
Pages (from-to)2896-2903
Number of pages8
JournalJournal of Applied Physiology
Volume74
Issue number6
StatePublished - Jan 1 1993

Fingerprint

T-kinin
Bradykinin B2 Receptors
Venules
Cheek
Mast Cells
Neurokinin-1 Receptor Antagonists
Histamine Release
Microcirculation
Indomethacin
Cricetinae

Keywords

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

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Gao, X. P., Mayhan, W., Conlon, J. M., Rennard, S. I., & Rubinstein, I. (1993). Mechanisms of T-kinin-induced increases in macromolecule extravasation in vivo. Journal of Applied Physiology, 74(6), 2896-2903.

Mechanisms of T-kinin-induced increases in macromolecule extravasation in vivo. / Gao, X. P.; Mayhan, William; Conlon, J. M.; Rennard, Stephen Israel; Rubinstein, I.

In: Journal of Applied Physiology, Vol. 74, No. 6, 01.01.1993, p. 2896-2903.

Research output: Contribution to journalArticle

Gao, XP, Mayhan, W, Conlon, JM, Rennard, SI & Rubinstein, I 1993, 'Mechanisms of T-kinin-induced increases in macromolecule extravasation in vivo', Journal of Applied Physiology, vol. 74, no. 6, pp. 2896-2903.
Gao, X. P. ; Mayhan, William ; Conlon, J. M. ; Rennard, Stephen Israel ; Rubinstein, I. / Mechanisms of T-kinin-induced increases in macromolecule extravasation in vivo. In: Journal of Applied Physiology. 1993 ; Vol. 74, No. 6. pp. 2896-2903.
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