단계적 요관압 상승시 신혈류량 증가에 대한 기전

Although tubuloglomerular feedback(TGF) is involved in ureteral obstruction-induced increase in renal blood flow(RBF), its contribution to RBF is not well established due to the concommitant increases in prostaglandin(PG) and renal interstitial fluid pressure (Pisf), both of which affect RBF one way or the other. Since Pisf and TGF are closely affected by renal hemodynamics, RBF will respond differently to increases in ureteral pressure depending on renal hemodynamic conditions. Therefore, the purpose of the present study was to investigate how the changes in renal hemodynamics affect the response of RBF to increases in ureteral pressure. The effect of PG on RBF was assessed by comparing the effects obtained before and after indomethacin, a cyclooxygenase inhibitor. Six anesthetized dogs were prepared with flow probes and inflatable silastic occluder around the renal artery, the ureteral catheter with its free end attached to a water reservoir, and the arterial and venous catheters. RBFs were obtained at ureteral pressures of 0, 15, and 40cmH2O during the maintenance of the renal artery pressure(RAP) at the level of systemic arterial pressure, 10mmHg above and below the lower autoregulatory limit of RBF(65±4 mmHg) both before and after indomethacin administration(10mg/kg). In response to the ureteral pressure of 40cmH2O, RBF increased from 172±6 to 185±10ml/min when RAP's were equal to systemic arterial pressure and decreased from 162±10 to 120±9 ml/min when RAP's were 55±4mmHg. Indomethacin pretreatment, depending on the level of RAP either prevented an increase or augmented a decrease in RBF in response to ureteral pressure elevation. This suggests that RAP-dependent changes in susceptibility of the renal venous system to compression by increased Pisf is the main mechanism by which the changes in renal perfusion pressure modulate the response of RBF to ureteral pressure elevation.