The Role of Protein Kinase C Epsilon in Hydrogen Peroxide and Nitric Oxide Release During Oxidative Stress Caused by Extracorporeal Shockwave Lithotripsy

摘要: The Role of Protein Kinase C Epsilon on Hydrogen Peroxide and Nitric Oxide Release during Oxidative Stress caused by Extracorporeal Shock Wave Lithotripsy Clinical extracorporeal shock wave lithotripsy (ESWL) treatment to ablate kidney stones can cause acute damage the renal microvasculature. Accumulation continued with shockwave therapy lead chronic kidney, clinical hypertension. Shockwaves have been shown stimulate endothelial cells release superoxide (SO), which is converted hydrogen peroxide (H2O2), reacts nitric oxide (NO) produce peroxynitrite anion (OONO ), creating a powerful oxidant that increases oxidative stress while simultaneously reducing NO bioavailability. Increased events such as ESWL, also uncouples production reaction in synthase (eNOS), causing eNOS SO instead NO, exacerbating insult. an essential signaling molecule responsible for vasodilation, functions inhibiting platelet adhesion leukocyte-endothelial interactions. This increased stress, decreased bioavailability, direct physical force causes prolonged vasodilation eventually vascular dysfunction vasculature. kinase epsilon (PKC-e) positively regulates eNOS, increasing its activity regardless whether producing or NO. We hypothesized PKC-e peptide inhibitor (N-Myr-EAVSLKPT, MW = 1054) would attenuate ESWLinduced H2O2 increase compared ESWL-saline control rats, activator (N-Myr-HDAPIGYD, 1097) ESWL-induced reduce release. was