Role of newly discovered endothelin-1(1-31) on renal injury

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1) Synthetic endothelin (ET)-1(1-31) decreased the lumen diameter of microperfused rabbit renal afferent and efferent arterioles, dose-dependently. ET-1(1-31)-induced renal arteriolar vasoconstriction was not influenced by phosphoramidon, an endothelin converting enzyme inhibitor. ET-1(1-31) exhibited vasoactive properties through ETィイD2AィエD2 or ETィイD2AィエD2-like receptors.2) ET-1(1-31) increased intracellular CaィイD12+ィエD1 in cultured human mesangial cell(HMC). The physiological activity of ET-1(1-31) may be attributable to CaィイD12+ィエD1 mobilization from intracellular stores rater than influx of CaィイD12+ィエD1 from extracellular space in HMC.3) ET-1(1-31) caused an increase in [ィイD13ィエD1H]-thymidine incorporation into the HMCs in a concentration-dependent manner. ET-1(1-31) itself stimulates HMC proliferation probably through endothelin ETィイD2AィエD2 or ETィイD2AィエD2-like receptors. The underlining mechanism of mesangial cell growth by ET-1(1-31) may be explained in part by PKC-dependent ERK1/2 activation.4) Plasma concentrations of immunoreactive ET-1(1-31) and ET-1 in healthy young volunteers were 1.70±0.23 pg/mL and 2.02±0.16 pg/mL, respectively. The plasma concentration level of ET-1(1-31) was equal to that of ET-1 in healthy young humans.