Nitric oxide and prostacyclin play a role in the regulation of microvascular protein and hydraulic permeability in cat skeletal muscle

Objective: To evaluate a possible role of nitric oxide (NO) and prostacyclin in the regulation of basal microvascular protein and hydraulic permeability. Methods: The study was performed on the autoperfused cat calf muscle. Changes in the osmotic reflection coefficient for albumin, calculated from the extended Starling equation, were used as a measure of altered protein permeability, whereas changes in capillary filtration coefficient (CFC) were used as a measure of altered hydraulic permeability. Results: Inhibition of the endogenous NO production with L-nitro-arginine methyl ester given intra-arterially to the muscle decreased the reflection coefficient to 70% of the control (p < 0.05) and increased the CFC by 17% (p < 0.05). The addition of a simultaneous intra-arterial infusion of the NO precursor L-arginine restored both the reflection coefficient and the CFC back to control level. Blockade of the endogenous prostacyclin production with tranylcypromine given intra-arterially decreased the reflection coefficient to 72% of the control (p < 0.05) and increased the CFC by 24% (p < 0.05), and they were both restored to control levels by a simultaneous intravenous infusion 4 a nonvasodilating dose of prostacyclin (1.0 ng/kg per minute). Conclusions: The results support the view that endogenous NO and prostacyclin decrease both protein and hydraulic permeability. Assuming a dynamic endogenous release of these substances, they may act as bidirectional regulators of protein and hydraulic permeability.