Lieberthal W, Arbeit L, Oza N B, Bernard D B, Levinsky N G
Hypertension. 1983 Jul-Aug;5(4):603-9. doi: 10.1161/01.hyp.5.4.603.
Urinary kallikrein excretion was studied in 34 patients with mild, normal-renin, essential hypertension without evidence of target organ damage and in 23 normotensive controls, using assays that measure both active (kininogenase activity) and total (active plus inactive) kallikrein. There was no significant difference in either active or total kallikrein excretion between the two groups. However, the ratio of active-to-total enzyme was decreased in the hypertensives (0.83 +/- 0.03 units/micrograms) compared to the normotensives (1.00 +/- 0.05 units/micrograms) (p less than 0.002). The active-to-total ratio was inversely related to sodium excretion in both groups, indicating that the proportion of active to inactive enzyme increased in response to reduced sodium intake. We conclude that, although absolute excretion of active and total kallikrein is not decreased, enzyme activity per microgram of total kallikrein excreted is reduced in mild, normal-renin essential hypertension. This abnormality may be due to a defective enzyme, or to a reduced excretion of active relative to inactive kallikrein. The latter could result from the presence of a urinary kallikrein inhibitor or to reduced activation of a proenzyme.
我们采用了能同时检测活性(激肽原酶活性)和总(活性加非活性)激肽释放酶的检测方法,对34例轻度、正常肾素型原发性高血压且无靶器官损害证据的患者以及23例血压正常的对照者的尿激肽释放酶排泄情况进行了研究。两组间活性或总激肽释放酶排泄均无显著差异。然而,与血压正常者(1.00±0.05单位/微克)相比,高血压患者的活性与总酶的比率降低(0.83±0.03单位/微克)(p<0.002)。两组中活性与总比率均与钠排泄呈负相关,表明随着钠摄入量减少,活性与非活性酶的比例增加。我们得出结论,尽管活性和总激肽释放酶的绝对排泄量并未降低,但在轻度、正常肾素型原发性高血压患者中,每微克排泄的总激肽释放酶的酶活性降低。这种异常可能是由于酶有缺陷,或者是活性激肽释放酶相对于非活性激肽释放酶的排泄减少。后者可能是由于存在尿激肽释放酶抑制剂,或者是前体酶的激活减少所致。