Abe K, Haruyama T, Sato M, Imai Y, Yasujima M, Seino M, Chiba S, Hiwatari M, Kasai Y, Tajima J, Itoh S, Yoshinaga K
Adv Exp Med Biol. 1983;156 (Pt B):977-84.
The present study was performed to investigate the roles of renal kallikrein and prostaglandin (PG) E in the mechanism of the exaggerated fractional Na excretion in hypertensive patients with advanced renal disease by means of the determination of urinary excretion of kallikrein and PGE, and fractional Na excretion in 20 healthy volunteers and 41 patients with chronic glomerulonephritis (14 normotensive patients; 9 borderline hypertensive patients; 18 sustained hypertensive patients). Urinary excretion of kallikrein and PGE was significantly decreased in patients with sustained hypertension as compared with healthy volunteers, while not decreased in those with normotensive or borderline hypertensive patients. Four times higher values for the fractional Na excretion and four or five times higher values for the urinary excretion of PGE corrected for creatinine clearance, were found in patients with borderline or sustained hypertension. There was a significant positive correlation (r = 0.6777) between the two. These results suggest that PGE in the renal tubular compartment may be involved in the mechanism of the exaggerated fractional Na excretion in patients with advanced renal disease. The urinary excretion rate of kallikrein corrected by creatinine clearance was three times greater in patients with borderline hypertension, but no significantly increase in those with sustained hypertension compared with that in healthy volunteers. There was no significant correlation between the fractional Na excretion and urinary kallikrein excretion corrected for creatinine clearance.
本研究旨在通过测定20名健康志愿者以及41例慢性肾小球肾炎患者（14例血压正常患者、9例临界高血压患者、18例持续性高血压患者）的尿激肽释放酶、前列腺素E（PGE）排泄量以及钠排泄分数，探讨肾脏激肽释放酶和前列腺素E（PGE）在晚期肾病高血压患者钠排泄分数增加机制中的作用。与健康志愿者相比，持续性高血压患者的尿激肽释放酶和PGE排泄量显著降低，而血压正常或临界高血压患者则未降低。临界或持续性高血压患者的钠排泄分数值高出四倍，经肌酐清除率校正后的PGE尿排泄量高出四到五倍。两者之间存在显著正相关（r = 0.6777）。这些结果表明，肾小管中的PGE可能参与了晚期肾病患者钠排泄分数增加的机制。经肌酐清除率校正后，临界高血压患者的尿激肽释放酶排泄率比健康志愿者高三倍，但持续性高血压患者与健康志愿者相比无显著增加。经肌酐清除率校正后的钠排泄分数与尿激肽释放酶排泄量之间无显著相关性。
