Geller R G, Margolius H S, Pisano J J, Keiser H R
Circ Res. 1975 Jun;36(6 Suppl 1):103-6. doi: 10.1161/01.res.36.6.103.
Urinary kallikrein was similar in 16-week-old Wistar/Kyoto (W/Ky) and spontaneously hypertensive (SH) rats, but at 23 weeks the SH rats excreted significantly less kallikrein. When dietary sodium was restricted, kallikrein excretion increased in the W/Ky but not in the SH rats. On high dietary sodium the opposite occurred: kallidrein excretion increased in the SH but not in the W/Ky rats. The pattern of urinary kallikrein excretion has some similarity to that seen in human hypertensive disease, i.e., the SH rat excretes less kallikrein than the normotensive control at 23 weeks of age and does not show an increased excretion when fed a low sodium diet. However, the rise in kallikrein shown by the SH rat on a high sodium diet is unique for this hypertensive model.
16周龄的Wistar/Kyoto(W/Ky)大鼠和自发性高血压(SH)大鼠的尿激肽释放酶水平相似,但在23周时,SH大鼠排泄的激肽释放酶显著减少。当限制饮食中的钠时,W/Ky大鼠的激肽释放酶排泄增加,而SH大鼠则没有。在高钠饮食时则出现相反的情况:SH大鼠的激肽释放酶排泄增加,而W/Ky大鼠则没有。尿激肽释放酶排泄模式与人类高血压疾病中的情况有一些相似之处,即SH大鼠在23周龄时排泄的激肽释放酶比正常血压对照大鼠少,并且在喂食低钠饮食时激肽释放酶排泄没有增加。然而,SH大鼠在高钠饮食时激肽释放酶的升高在这个高血压模型中是独特的。