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Am J Physiol Heart Circ Physiol 277: H152-H160, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 1, H152-H160, July 1999

Concentration-dependent effects of bradykinin on leukocyte recruitment and venular hemodynamics in rat mesentery

Sakuji Shigematsu, Shuji Ishida, Dean C. Gute, and Ronald J. Korthuis

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 (>= 10-6 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


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