Buck A C, Sampson W F, Lote C J, Blacklock N J
Br J Urol. 1981 Dec;53(6):485-91. doi: 10.1111/j.1464-410x.1981.tb03244.x.
In a clinical study of 275 idiopathic stone formers the GFR was significantly raised in hypercalciuric patients compared with normal controls P less than 0.001). The possibility that the mechanism underlying hypercalciuria and raised GFR may be prostaglandin-mediated was considered because it is now well established that prostaglandins regulate intra-renal haemodynamics and influence tubular electrolyte excretion. Experiments were performed in conscious Sprague Dawley rats to determine the changes in calcium and sodium excretion following prostaglandin synthetase inhibition with indomethacin. Both calcium and sodium excretion together with urine flow were significantly reduced (P less than 0.002). Further experiments were performed in anaesthetised monkeys (Macacca fascicularis) to see if the inhibitory effect of indomethacin was reversible. Exogenous prostaglandin (PGE2) infusion resulted in a marked calciuretic response without producing changes in GFR or blood pressure. Selected hypercalciuric patients were treated with indomethacin, which resulted in a significant fall in urinary calcium excretion (P less than 0.001). This clinical and experimental study suggests that PGE2 is the hormone which determines the renal handling of calcium by controlling renal tubular function.
在一项针对275名特发性结石形成者的临床研究中，与正常对照组相比，高钙尿症患者的肾小球滤过率（GFR）显著升高（P<0.001）。由于现已充分证实前列腺素可调节肾内血流动力学并影响肾小管电解质排泄，因此考虑高钙尿症和升高的GFR背后的机制可能是前列腺素介导的。对清醒的斯普拉格-道利大鼠进行实验，以确定用吲哚美辛抑制前列腺素合成酶后钙和钠排泄的变化。钙和钠排泄以及尿流量均显著降低（P<0.002）。在麻醉的猕猴（食蟹猴）身上进行了进一步实验，以观察吲哚美辛的抑制作用是否可逆。输注外源性前列腺素（PGE2）导致明显的利钙反应，而GFR或血压未发生变化。选择的高钙尿症患者用吲哚美辛治疗，导致尿钙排泄显著下降（P<0.001）。这项临床和实验研究表明，PGE2是一种通过控制肾小管功能来决定肾脏对钙处理的激素。
