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We hypothesize that ESWL treatment will decrease NO and increase H2O2 release in rat renal veins compared to no-ESWL controls. We further hypothesize that a postESWL i.v. bolus of PKCe+/BH4 will increase NO and decrease H2O2 release compared to ESWL + saline controls. Whereas, we expect a post-ESWL i.v. infusion of PKCe+/BH2 will decrease NO and increase H2O2 compared to ESWL + saline controls. We hypothesize that PKCegiven with either BH4 or BH2 after ESWL will increase NO and decrease H2O2 release compared to ESWL + saline controls. ESWL treatment decreased NO and increased H2O2 blood levels compared to noESWL controls. This supports our hypothesis and previous findings in this lab that ESWL causes oxidative stress and reduced NO bioavailability. Post-ESWL PKCe+/BH4 significantly attenuated the adverse effects of ESWL by increasing NO and decreasing H2O2 release compared to ESWL+saline. This suggests that this combination enhances eNOS in its coupled state. Whereas, post-ESWL PKCe+/BH2 was similar to ESWL control in H2O2 and NO, suggesting that BH2 is nearing saturation to the eNOS binding site. In contrast, post-ESWL PKCewith either BH4 or BH2 resulted in increased NO and decreased H2O2 compared to ESWL+saline. This suggests that PKCeattenuates eNOS uncoupled activity after ESWL. Potentially, this study can help to develop therapeutic uses for PKCe+/BH4 or PKCein the attenuation of vascular endothelial dysfunction following ESWL treatment and possibly eliminate or reduce the acute renal complications that may lead to chronic conditions such as hypertension. Results

The Effects of Modulating Endothelial Nitric Oxide Synthase (eNOS) Activity and Coupling in Extracorporeal Shock Wave Lithotripsy (ESWL)