血管紧张素、去甲肾上腺素、血管加压素和醛固酮对大鼠尿激肽释放酶排泄的影响。
Effect of angiotensin, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion in the rat.
作者信息
Catanzaro O L, Martinez Seeber A, Vila S B
出版信息
Pharmacol Res Commun. 1984 Aug;16(8):775-83. doi: 10.1016/s0031-6989(84)80054-5.
In male Wistar rats, under osmotic diuresis, the effect of angiotensin II, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion were evaluated. Angiotensin II did not modify but all the others drugs used increased significantly the urinary kallikrein excretion. In all the groups studied the urinary sodium excretion increased. No modifications were observed in urine flow, glomerular filtration rate, urine osmolality and potassium excretion. The urinary kallikrein excretion was always positively correlated with the urinary flow and urinary sodium excretion. No correlation was observed with the other parameters studied. These findings suggest that noradrenaline, vasopressin and aldosterone are important stimulators of the urinary kallikrein excretion. Probably, kallikrein is one of the mechanisms involved in the regulation of urinary sodium excretion.
在雄性Wistar大鼠中，在渗透性利尿情况下，评估了血管紧张素II、去甲肾上腺素、血管加压素和醛固酮对尿激肽释放酶排泄的影响。血管紧张素II没有改变，但所用的其他所有药物均显著增加了尿激肽释放酶的排泄。在所有研究组中，尿钠排泄均增加。尿流量、肾小球滤过率、尿渗透压和钾排泄均未观察到改变。尿激肽释放酶排泄始终与尿流量和尿钠排泄呈正相关。与所研究的其他参数未观察到相关性。这些发现表明，去甲肾上腺素、血管加压素和醛固酮是尿激肽释放酶排泄的重要刺激物。激肽释放酶可能是参与尿钠排泄调节的机制之一。
Zotero 插件