Zoja C, Benigni A, Renzi D, Piccinelli A, Perico N, Remuzzi G
Mario Negri Institute for Pharmacological Research, Bergamo, Italy.
Kidney Int. 1990 Mar;37(3):927-33. doi: 10.1038/ki.1990.67.
We investigated the effect of endothelin on the generation of eicosanoids, which are known to regulate basal and stimulated mesangial cell tone. The results showed that endothelin is a potent stimulus of prostaglandin E2 (PGE2), prostacyclin (PGI2), and thromboxane A2 (TxA2) synthesis by bovine mesangial cells. Percentage increases in eicosanoid synthesis induced by endothelin (10(-10) to 10(-6) M), were 50 to 275% for PGE2, 28 to 168% for PGI2 and 42 to 111% for TxA2, respectively. Endothelin-induced eicosanoid synthesis in mesangial cells was concentration, but not time dependent. Aspirin (500 microM) completely prevented endothelin-induced eicosanoid synthesis. The calcium entry blocker nitrendipine (10(-8) M) failed to inhibit endothelin-induced eicosanoid synthesis. These data suggest that endothelin-induced changes in renal circulation and glomerular function in normal and disease conditions may be modulated by the concomitant stimulation of mesangial eicosanoid synthesis.
我们研究了内皮素对类花生酸生成的影响，已知类花生酸可调节系膜细胞的基础张力和刺激后的张力。结果表明，内皮素是牛系膜细胞合成前列腺素E2（PGE2）、前列环素（PGI2）和血栓素A2（TxA2）的有效刺激物。内皮素（10^(-10)至10^(-6)M）诱导的类花生酸合成百分比增加，PGE2为50%至275%，PGI2为28%至168%，TxA2为42%至111%。内皮素诱导的系膜细胞类花生酸合成与浓度有关，但与时间无关。阿司匹林（500微摩尔）完全阻止了内皮素诱导的类花生酸合成。钙通道阻滞剂尼群地平（10^(-8)M）未能抑制内皮素诱导的类花生酸合成。这些数据表明，在正常和疾病状态下，内皮素诱导的肾循环和肾小球功能变化可能受到系膜类花生酸合成同时刺激的调节。
