Overlack A, Stumpe K O, Müller H M, Kolloch R, Higuchi M
Klin Wochenschr. 1982 Oct 1;60(19):1223-8. doi: 10.1007/BF01716727.
The renal kallikrein-kinin system may participate in the diuretic, natriuretic and antihypertensive effect of diuretics. This possibility was investigated by studying the influence of hydrochlorothiazide on blood pressure and urinary kallikrein excretion in patients with essential hypertension. Furthermore, the effect of kallikrein-blockade and prostaglandin-synthesis inhibition on the acute furosemide-induced changes of diuresis, natriuresis, GFR and renal plasma flow were studied in normotensive subjects. Thiazide treatment normalized the reduced kallikrein excretion of the hypertensive patients. The fall in mean arterial blood pressure was significantly correlated with the increase in urinary kallikrein excretion. In the normotensive subjects aprotinin-induced kallikrein inhibition failed to alter the acute response to furosemide, whereas indomethacin attenuated the diuretic and natriuretic effect of furosemide. The combination of indomethacin and aprotinin had a greater suppressive effect on plasma renin activity than indomethacin alone, suggesting a participation of kallikrein in renin release. An increase in the activity of the renal kallikrein-kinin system may contribute to the long-term antihypertensive effect of thiazide diuretics but it does not seem to be involved in the acute renal responses to furosemide.
肾激肽释放酶 - 激肽系统可能参与利尿剂的利尿、排钠和降压作用。通过研究氢氯噻嗪对原发性高血压患者血压和尿激肽释放酶排泄的影响来探讨这种可能性。此外，还研究了在血压正常的受试者中，激肽释放酶阻断和前列腺素合成抑制对速尿急性诱导的利尿、排钠、肾小球滤过率（GFR）和肾血浆流量变化的影响。噻嗪类治疗使高血压患者减少的激肽释放酶排泄恢复正常。平均动脉血压的下降与尿激肽释放酶排泄的增加显著相关。在血压正常的受试者中，抑肽酶诱导的激肽释放酶抑制未能改变对速尿的急性反应，而吲哚美辛减弱了速尿的利尿和排钠作用。吲哚美辛和抑肽酶联合使用对血浆肾素活性的抑制作用比单独使用吲哚美辛更大，提示激肽释放酶参与肾素释放。肾激肽释放酶 - 激肽系统活性的增加可能有助于噻嗪类利尿剂的长期降压作用，但似乎不参与对速尿的急性肾反应。
