Obika L F
Arch Int Physiol Biochim. 1987 Mar;95(1):13-8. doi: 10.3109/13813458709075020.
The relationship of urinary kallikrein excretion to urine volume, and to urinary sodium and potassium excretions was studied in normal rats during furosemide diuresis and superimposed injection of amiloride, a K+-sparing diuretic. Continuous infusion of furosemide increased urinary kallikrein, sodium and potassium excretions and the urine volume. Amiloride injection during furosemide diuresis caused further increase in diuresis and natriuresis, but a prompt decrease in urinary kallikrein excretion to basal level, and potassium excretion to below the basal level. The significant correlation of urinary kallikrein excretion to urinary potassium excretion, but not to urine volume and urinary sodium excretion after amiloride injection suggests that the major determinant of urinary kallikrein excretion is renal potassium secretion through a mechanism that is affected by amiloride.
在速尿利尿期间及叠加注射保钾利尿剂氨氯吡咪的情况下，研究了正常大鼠尿激肽释放酶排泄量与尿量、尿钠及尿钾排泄量之间的关系。持续输注速尿可增加尿激肽释放酶、钠和钾的排泄量以及尿量。在速尿利尿期间注射氨氯吡咪会使利尿和利钠作用进一步增强，但尿激肽释放酶排泄量迅速降至基础水平，钾排泄量降至基础水平以下。氨氯吡咪注射后，尿激肽释放酶排泄量与尿钾排泄量显著相关，而与尿量和尿钠排泄量无关，这表明尿激肽释放酶排泄的主要决定因素是通过一种受氨氯吡咪影响的机制进行的肾脏钾分泌。
