Sipilä R, Jalkanen M, Huotari K
Ann Clin Res. 1986;18(4):208-10.
To study the urinary kallikrein excretion before the delivery of term pregnancy we measured its excretion preterm (between 32-36 gestational week) in 13 patients with normotensive pregnancy and 17 patients with pregnancy-induced hypertension and one to five days before the delivery at term in 18 and 22 patients, respectively. In normotensive pregnancy urinary kallikrein excretion remained unchanged during the late third trimester until delivery (12.6 +/- 1.7 ncat in 24 hours in preterm, 10.8 +/- 1.2 before delivery). In pregnancy-induced hypertension and particularly in pre-eclampsia urinary kallikrein excretion was lower than in normotensive pregnancy and the decrease became more marked as the time of delivery approached (respective values: in pregnancy induced hypertension 9.2 +/- 1.2 and 7.0 +/- 0.7; in pre-eclampsia 7.6 +/- 1.3 and 7.3 +/- 0.9). The decrease in urinary kallikrein excretion suggests progressive disturbances in the interactions of renal vasoactive systems (the kallikrein-kinin system, the renin-angiotensin system and prostaglandins) with resultant changes in renal hemodynamics.
为研究足月妊娠分娩前的尿激肽释放酶排泄情况,我们分别测定了13例血压正常孕妇在早产时(孕32 - 36周)以及18例和22例孕妇在足月分娩前1至5天的尿激肽释放酶排泄量,其中17例为妊娠高血压患者。在血压正常的妊娠中,妊娠晚期直至分娩期间尿激肽释放酶排泄量保持不变(早产时24小时为12.6±1.7纳卡特,分娩前为10.8±1.2)。在妊娠高血压尤其是先兆子痫患者中,尿激肽释放酶排泄量低于血压正常的妊娠,且随着分娩时间临近,这种降低变得更加明显(具体数值:妊娠高血压患者分别为9.2±1.2和7.0±0.7;先兆子痫患者为7.6±1.3和7.3±0.9)。尿激肽释放酶排泄量的降低表明肾血管活性系统(激肽释放酶 - 激肽系统、肾素 - 血管紧张素系统和前列腺素)之间的相互作用逐渐紊乱,从而导致肾血流动力学发生变化。