Endothelial cells (EC) participate in leukocyte adhesion and transmigration, and venular hyperpermeability, typical events of inflammation. EC are communicated and electrically coupled to each other by gap junction channels (GJ). The formation of endothelial-leukocyte heterotypic GJ has also been documented in vitro, however the possible function of GJ in the inflammatory response is not established. Male Golden Syrian Hamsters (115 ± 10 g, mean ± sem) were anesthetized with pentobarbital sodium (65 mg kg^-1 I.P.) and the cheek pouch microcirculation was exposed, superfused and observed by intravital microscopy. Inflammation was induced by a topical application of PAF (10^-7 M) for 5 min, either in the presence (n=9) or absence (n=7) of a GJ blocker, α-glycyrrhetinic acid (AGA, 75 μM). Arteriolar diameter was registered every 5 min. Macromolecular leakage was determined by the clearance of FITC-dextran 150 kDa during 90 min, starting 30 min before PAF. Leukocyte adhesion and transmigration was registered every 15 min. Animals were maintained under deep anaesthesia with supplementary doses of pentobarbital sodium (20 mg kg^-1 I.V.) as required, and were killed with an anaesthetic overdose (300 mg kg^-1 I.V.) at the end of the experiment. PAF produced transitory arteriolar constriction, peaking 5 min post stimulus. Diameter decreased by 45 ± 10 % in A4 arterioles (5-15 μm, n=13), while it decreased by 24 ± 8 % in A3 arterioles (15-30 μm, n=12). PAF-induced arteriolar constriction was not modified in presence of AGA (42 ± 6 % in A4, n=20, and 25 ± 8 % in A3, n=12). Stimulation with PAF increased macromolecular leakage, which reached a maximum approximately ten-fold over baseline 25 min post stimulation. PAF-induced increase in dextran clearance was not changed during AGA application. In control, PAF application induced a steady rise in the number of leukocytes adhered to venular endothelium, which reached 10.0 ± 0.9 cells per 100 μm of vessel length at 60 min post stimulus (n=7). Interestingly, AGA abolished the effect of PAF on leukocyte adhesion, the number of sticking cells at 60 min post stimulus was 2.4 ± 0.3 per 100 μm (n=9, p<0.05 vs control, equal to tissues non-stimulated, n=7, or treated with AGA alone, n=6, two-way ANOVA). Similarly, AGA reduced the extent of transmigrated leukocytes observed 60 min post PAF (4.1 ± 0.3 vs 5.9 ± 0.9, cells per 104 μm², p<0.05). These results indicate that GJ are important for the initiation and development of leukocyte adhesion and transmigration, confirming previous results from our laboratory obtained with other pro-inflammatory stimulus. However, the data do not support that GJ participate in other microvascular inflammatory effects induced by PAF.