Vernace M A, Mento P F, Maita M E, Girardi E P, Chang M D, Nord E P, Wilkes B M
Department of Medicine, North Shore University Hospital, Manhasset, New York 11030, USA.
J Clin Invest. 1995 Jul;96(1):183-91. doi: 10.1172/JCI118019.
We tested the hypothesis that endothelin (ET) responsiveness in the renal medulla is modulated by ambient osmolarity. Cultured renal medullary interstitial cells (RMICs) were incubated from 3 to 24 h in isosmolar culture medium (300 mOsm/kg H2O) or media rendered hyperosmolar (600 mOsm/kg H2O) by the addition of urea. Under hyperosmolar conditions, the peak of ET-evoked Ca2+ transient was blunted by 45-58% (P < 0.02) and PGE2 accumulation decreased from 16- to 2-fold above basal values (P < 0.001). To explore whether hyperosmolar conditions blunt intracellular signaling via modulation of receptor number or expression, kinetics of ET binding and Northern blot analysis of ETA receptor mRNA was performed. Under hyperosmolar conditions, ETA receptor density was reduced by 84% versus isosmolar conditions (238 +/- 12 vs. 1450 +/- 184 fmol/mg) (P < 0.01). In contrast to the ligand binding studies, ETA receptor mRNA was increased by 58% (P < 0.05) in cells grown under hyperosmolar versus isosmolar media. These observations indicate that in the hyperosmolar setting, ET-evoked intracellular signaling is blunted in RMICs due to ET receptor downregulation. Since ETA receptor mRNA is increased under hyperosmolar conditions, we conclude that ET receptor downregulation is the consequence of either decreased translation of message, increased degradation of receptor peptide, or increased internalization of specific receptor sites.
肾髓质中内皮素(ET)的反应性受周围渗透压的调节。将培养的肾髓质间质细胞(RMICs)在等渗培养基(300 mOsm/kg H₂O)中孵育3至24小时,或通过添加尿素使其变为高渗培养基(600 mOsm/kg H₂O)。在高渗条件下,ET诱发的Ca²⁺瞬变峰值降低了45 - 58%(P < 0.02),前列腺素E₂(PGE₂)的积累从高于基础值的16倍降至2倍(P < 0.001)。为探究高渗条件是否通过调节受体数量或表达来减弱细胞内信号传导,我们进行了ET结合动力学研究以及ETA受体mRNA的Northern印迹分析。在高渗条件下,与等渗条件相比,ETA受体密度降低了84%(238 ± 12对1450 ± 184 fmol/mg)(P < 0.01)。与配体结合研究结果相反,在高渗培养基中生长的细胞中,ETA受体mRNA增加了58%(P < 0.05)。这些观察结果表明,在高渗环境中,RMICs中ET诱发的细胞内信号传导因ET受体下调而减弱。由于在高渗条件下ETA受体mRNA增加,我们得出结论,ET受体下调是以下原因造成的:要么是信息翻译减少,要么是受体肽降解增加,要么是特定受体位点的内化增加。