Sato M, Abe K, Haruyama T, Yasujima M, Sato K, Chiba S, Imai Y, Hiwatari M, Kasai Y, Tajima J, Itoh S, Seino M, Goto T, Yoshinaga K
Prostaglandins Leukot Med. 1982 Mar;8(3):199-209. doi: 10.1016/0262-1746(82)90043-9.
To investigate the role of renal prostaglandins (PGs) in the renal handling of sodium, urinary excretion of PGE, PGF2 alpha and PGF2 alpha MUM (main urinary metabolite of PGF2 alpha) were measured after various manipulations of dietary sodium intake in 8 hypertensive patients. A low sodium intake increased urinary excretion of PGF2 alpha MUM (p less than 0.05), but failed to change urinary excretion of PGE and PGF2 alpha. In contrast, a high sodium intake increased urinary excretion of PGE (p less than 0.01) and decreased urinary excretion of PGF2 alpha MUM (p less than 0.02). A low sodium intake decreased the ratio of urinary PGE/PGF2 alpha MUM and high sodium increased it (both p less than 0.001). There was a significant positive correlation between urinary excretion of sodium and that of PGE (p less than 0.001). Additional oral administration of potassium chloride did not change urinary excretion of PGs. These results may suggest that dietary sodium intake may be one of the regulators of the metabolism of PGs in the kidney, supporting the hypothesis that renal PGE has a natriuretic action in humans.
为研究肾前列腺素(PGs)在肾脏钠处理中的作用,对8例高血压患者进行不同饮食钠摄入量处理后,测定了尿中PGE、PGF2α及PGF2α MUM(PGF2α的主要尿代谢产物)的排泄量。低钠饮食增加了PGF2α MUM的尿排泄量(p<0.05),但未改变PGE和PGF2α的尿排泄量。相反,高钠饮食增加了PGE的尿排泄量(p<0.01),并降低了PGF2α MUM的尿排泄量(p<0.02)。低钠饮食降低了尿中PGE/PGF2α MUM的比值,高钠饮食则使其升高(两者p<0.001)。尿钠排泄量与PGE排泄量之间存在显著正相关(p<0.001)。额外口服氯化钾未改变PGs的尿排泄量。这些结果可能提示饮食钠摄入量可能是肾脏中PGs代谢的调节因子之一,支持了肾PGE在人类中具有利钠作用这一假说。