Abstract: Objective: To study the effect of endothelial [Ca2+]i and NO production on H2O2 induced increased mesenteric microvessel permeability in normal adult rats. Methods: Microvessel permeability was assessed by measuring hydraulic conductivity (Lp). H2O2-induced changes in endothelial [Ca2+]i and NO production were measured in Fura-2 AM (Ca2+ fluorescent indicator) or DAF-2 DA (NO fluorescent indicator) loaded microvessels in vivo via fluorescence microscopy. Results: H2O2 can increase mesenteric microvessel permability (6.13±0.87 times control value, P<0.01）and increase endothelial [Ca2+]i (714.58±144.70 nmol/L, P<0.01）and NO production (1034.3%±44.3% of control ?uorescence intensity, P<0.01)in normal adult rats. Calcium channel blocker, Lanthanum Chloride (LaCl3), inhibited the increase in microvessel permeability (P<0.01) and endothelial [Ca2+]i (P<0.01) induced by H2O2. NOS inhibitor, AP-Cav-1, can inhibit increased microvessel permeability induced by H2O2 (P<0.01), but have no effect on increased endothelial [Ca2+]i. Conclusion: Increased microvessel endothelial [Ca2+]i and NO production is involved in H2O2 induced increases in microvessel permeability.

Key words: hydrogen peroxide, permeability, endothelial cell, calcium, nitric oxide