| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, School of Medicine in Shreveport, Shreveport, Louisiana 71130
The results of several recent studies indicate
that bradykinin protects tissues against the deleterious effects of
ischemia-reperfusion (I/R). However, other studies indicate
that bradykinin can act as a proinflammatory agent, inducing P-selectin
expression, the formation of chemotactic stimuli, and endothelial
barrier disruption. In the present study, we used intravital
microscopic techniques to examine the dose-dependent effects of
bradykinin on leukocyte-endothelial cell interactions, the formation of
platelet-leukocyte aggregates, and venular hemodynamics in rat
mesentery in an attempt to explain these divergent findings.
Superfusion of the mesentery with low concentrations of bradykinin
(
10
7 M) increased venular
erythrocyte velocity
(VRBC) without
increasing the number of adherent leukocytes, whereas higher
concentrations (
106
M) decreased
VRBC, increased
the number of platelet-leukocyte aggregates, and induced leukocyte
adhesion in single postcapillary venules. The formation of
platelet-leukocyte aggregates and increased leukocyte adhesion induced
by high-dose bradykinin were attenuated by administration of a
B2-receptor (HOE-140) or a
platelet-activating factor (PAF, WEB-2086) antagonist. Thus these
adhesive interactions induced by high-dose bradykinin appear to be
mediated by a mechanism that is dependent on
B2-receptor activation and the
formation of PAF or PAF-like lipids. The effects of bradykinin on
venular VRBC and
blood flow were also concentration dependent, with low doses producing
nitric oxide-mediated vasodilation, whereas high doses decreased
VRBC by a
mechanism that is PAF independent.
leukocyte adhesion; postcapillary venules; erythrocyte velocity; B2 receptors; platelet-activating factor; nitric oxide synthase; cyclooxygenase
This article has been cited by other articles:
|
|
 |
|
  M. Yusof, K. Kamada, F. Spencer Gaskin, and R. J. Korthuis Angiotensin II mediates postischemic leukocyte-endothelial interactions: role of calcitonin gene-related peptide Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H3032 - H3037. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Shigematsu, S. Ishida, D. C. Gute, and R. J. Korthuis Bradykinin-induced proinflammatory signaling mechanisms Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2676 - H2686. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Shigematsu, S. Ishida, D. C. Gute, and R. J. Korthuis Postischemic anti-inflammatory effects of bradykinin preconditioning Am J Physiol Heart Circ Physiol, January 1, 2001; 280(1): H441 - H454. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. G. McLean, A. Ahluwalia, and M. Perretti Association between Kinin B1 Receptor Expression and Leukocyte Trafficking across Mouse Mesenteric Postcapillary Venules J. Exp. Med., July 31, 2000; 192(3): 367 - 380. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Shigematsu, S. Ishida, D. C. Gute, and R. J. Korthuis Bradykinin prevents postischemic leukocyte adhesion and emigration and attenuates microvascular barrier disruption Am J Physiol Heart Circ Physiol, July 1, 1999; 277(1): H161 - H171. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
