Modulation of the myogenic response in renal blood flow autoregulation by NO depends on endothelial nitric oxide synthase (eNOS), but not neuronal or inducible NOS

Non-Technical Summary  Blood flow in the kidney is tightly regulated. This so-called autoregulation is essential for the function of the kidney as well as for its protection against damage and failure from high blood pressure. Autoregulation is caused by three mechanisms. The signalling molecule nitric oxide (NO) modulates the balance of these mechanisms, blunting the contribution of the fastest mechanism and increasing that of the others. What is unknown is where in the kidney the responsible NO is originating. Our data indicate that the cells of the inner lining of the blood vessels are by far the most important source of NO for this effect compared to other NO-producing cells in the relevant region of the kidney, such as macula densa, smooth muscle or mesangial cells. The findings are important for understanding blood flow autoregulation in the kidney as well as kidney function and failure.