Purkerson M L, Klahr S
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.
Kidney Int. 1989 Jun;35(6):1305-14. doi: 10.1038/ki.1989.127.
The present studies were designed to analyze the potential contribution of angiotensin II and thromboxane A2 to the remarkable decrease in glomerular filtration rate (GFR) and renal plasma flow observed after unilateral release of 24-hour bilateral ureteral obstruction. Pretreatment of the animals with inhibitors of either thromboxane or angiotensin synthesis for 48 hours prior to and during obstruction eliminated the contribution of these vasoconstrictors. Inhibition of these vasoconstrictors during the period of obstruction results in a greater increase in renal plasma flow and GFR than when inhibition was accomplished after release of the obstruction. These data suggest a greater role for these vasoconstrictors in the decrease in GFR that occurs with obstruction. Simultaneous inhibition of thromboxane and angiotensin production normalized GFR of the postobstructed kidney. Administration of atrial peptide after release of obstruction in the different groups of rats resulted in further increases in GFR, urine flow and absolute sodium excretion. It is suggested that atrial peptide participates in the renal hemodynamic changes that occur in the postobstructed kidney.
本研究旨在分析血管紧张素II和血栓素A2对单侧解除24小时双侧输尿管梗阻后肾小球滤过率（GFR）和肾血浆流量显著下降的潜在作用。在梗阻前及梗阻期间，用血栓素或血管紧张素合成抑制剂对动物进行48小时预处理，可消除这些血管收缩剂的作用。在梗阻期间抑制这些血管收缩剂，与梗阻解除后进行抑制相比，肾血浆流量和GFR的增加幅度更大。这些数据表明，这些血管收缩剂在梗阻导致的GFR下降中起更大作用。同时抑制血栓素和血管紧张素的产生可使梗阻后肾脏的GFR恢复正常。在不同组大鼠梗阻解除后给予心房肽，可使GFR、尿流量和绝对钠排泄进一步增加。提示心房肽参与了梗阻后肾脏发生的肾血流动力学变化。
