Bönner G, Autenrieth R, Marin-Grez M, Speck G, Gross F
Acta Endocrinol (Copenh). 1984 Sep;107(1):131-40. doi: 10.1530/acta.0.1070131.
In male Sprague-Dawley rats the influence of salt loading (1% NaCl), deoxycorticosterone acetate (2 X 15 mg/kg/day resp. 250 mg/kg sc), corticosterone (2 X 20 mg/kg/day sc) and adrenocorticosterone (0.5 mg/kg/day tetracosactid sc) on the activity of renal kallikrein and renal renin activity was investigated. Salt loading lowered renal kallikrein activity, deoxycorticosterone stimulated its activity and in combination they had no effect on renal kallikrein activity. The time course of kallikrein stimulation by deoxycorticosterone showed no relationship to the escape phenomenon of the kidney from the sodium retaining effect of the mineralocorticoid hormone. Reduction of endogenous mineralocorticoid hormones by adrenalectomy caused a marked reduction of urinary and renal kallikrein activity. Corticosterone suppressed the activity of the renal kallikrein-kinin system at the same time as the reduction in urinary aldosterone excretion. Adrenocorticotrophin caused the same decrease in the activity of renal kallikrein as corticosterone. Urinary aldosterone excretion, however, was significantly stimulated. Thus, the known positive correlation between kallikrein and aldosterone was missing. In all experiments the urinary excretion of kallikrein correlated highly with the kallikrein activity measured in renal cortical tissue. However, no correlation was found between kallikrein and urine volume or urinary excretion of sodium and potassium. In our experiments no relationship between the activity of the renin-angiotensin system and that of the renal kallikrein-kinin system was observed. Furthermore, no clear relationship was found between systemic blood pressure and the activity of the renal kallikrein-kinin system.
在雄性Sprague-Dawley大鼠中，研究了盐负荷（1%氯化钠）、醋酸脱氧皮质酮（分别为2×15毫克/千克/天和250毫克/千克皮下注射）、皮质酮（2×20毫克/千克/天皮下注射）和促肾上腺皮质激素（0.5毫克/千克/天替可克肽皮下注射）对肾激肽释放酶活性和肾素活性的影响。盐负荷降低了肾激肽释放酶活性，脱氧皮质酮刺激了其活性，二者联合使用对肾激肽释放酶活性无影响。脱氧皮质酮刺激激肽释放酶的时间进程与肾脏对盐皮质激素钠潴留作用的逃逸现象无关。肾上腺切除减少内源性盐皮质激素导致尿和肾激肽释放酶活性显著降低。皮质酮在降低尿醛固酮排泄的同时抑制了肾激肽释放酶-激肽系统的活性。促肾上腺皮质激素导致肾激肽释放酶活性与皮质酮引起的降低相同。然而，尿醛固酮排泄受到显著刺激。因此，激肽释放酶与醛固酮之间已知的正相关关系不存在。在所有实验中，尿激肽释放酶排泄与肾皮质组织中测得的激肽释放酶活性高度相关。然而，未发现激肽释放酶与尿量或尿钠和钾排泄之间存在相关性。在我们的实验中，未观察到肾素-血管紧张素系统活性与肾激肽释放酶-激肽系统活性之间的关系。此外，未发现全身血压与肾激肽释放酶-激肽系统活性之间存在明确关系。
