Firth J D, Ratcliffe P J, Raine A E, Ledingham J G
Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford.
Lancet. 1988 Nov 19;2(8621):1179-82. doi: 10.1016/s0140-6736(88)90243-7.
Very low concentrations of the vasoconstrictor peptide endothelin cause intense long-lasting renal vasoconstriction. In the isolated perfused rat kidney, the concentration of endothelin required to reduce blood-flow by 50% is 200 pmol/l, compared with 1000 pmol/l angiotensin II (previously the most potent known vasoconstrictor). Whereas angiotensin II has little effect on the glomerular filtration rate (GFR), a rise in endothelin from 100 to 800 pmol/l reduces GFR by 90%. Endothelin is probably present in the circulation at low concentrations in vivo; events associated clinically with acute renal failure would tend to increase this concentration. Endothelin may be a mediator in the pathogenesis of acute renal failure.
极低浓度的血管收缩肽内皮素可引起强烈且持久的肾血管收缩。在离体灌注的大鼠肾脏中，使血流量减少50%所需的内皮素浓度为200皮摩尔/升，而血管紧张素II（此前已知最强效的血管收缩剂）则为1000皮摩尔/升。血管紧张素II对肾小球滤过率（GFR）影响甚微，而内皮素浓度从100皮摩尔/升升至800皮摩尔/升可使GFR降低90%。内皮素在体内循环中的浓度可能较低；临床上与急性肾衰竭相关的情况往往会使该浓度升高。内皮素可能是急性肾衰竭发病机制中的一种介质。
