Abe K, Yasujima M, Chiba S, Sato M, Irokawa N, Imai Y, Yoshinaga K
Adv Exp Med Biol. 1979;120B:487-501.
The present study was done to investigate the interrelationships between renal kallikrein-kinin, renal prostaglandin E and renin-angiotensin-aldosterone systems in normal subjects and in essential hypertension by means of measuring urinary excretion of kallikrein and prostaglandin E, plasma renin activity and plasma aldosterone concentration before and after stimulation or inhibition of the renin-angiotensin-aldosterone system and inhibition of renal prostaglandin E generation. Urinary kallikrein excretion was increased after the stimulation of the renin-angiotensin-aldosterone system by low Na diet or the administration of furosemide and upright posture, while it decreased after the inhibition of the action of aldosterone by spironolactone. These data show that the change in urinary kallikrein excretion was related to that in the renin-angiotensin-aldosterone system following various stimuli, suggesting that renal kallikrein-kinin system may regulate blood pressure by opposing the action of the renin-angiotensin-aldosterone system. Urinary PGE excretion was decreased after sodium depletion and increased after the administration of furosemide in spite of the augmentation of the renin-angiotensin-aldosterone system. The change in urinary PGE excretion was closely related to that in urinary Na output after various stimuli, and a significant positive correlation was found between basal levels of urinary PGE and those of urinary Na, suggesting that renal prostaglandin E may be involved in the regulation of blood pressure by affecting renal sodium handling. The present data show that basal level of urinary excretion of PGE and kallikrein was lower in essential hypertension than in normal subjects and that the release of renal kallikrein and PGE after the furosemide administration was also suppressed in patients with essential hypertension compared with that in normal subjects, suggesting that there exists, in this disease, an impaired defense mechanism against the renin-angiotensin-aldosterone system resulting in sodium retention.
本研究旨在通过测量正常人和原发性高血压患者在肾素 - 血管紧张素 - 醛固酮系统受刺激或抑制以及肾前列腺素E生成受抑制前后的尿激肽释放酶、前列腺素E的排泄量、血浆肾素活性和血浆醛固酮浓度，来研究肾激肽释放酶 - 激肽、肾前列腺素E和肾素 - 血管紧张素 - 醛固酮系统之间的相互关系。低钠饮食、服用呋塞米和直立姿势刺激肾素 - 血管紧张素 - 醛固酮系统后，尿激肽释放酶排泄增加，而螺内酯抑制醛固酮作用后，尿激肽释放酶排泄减少。这些数据表明，尿激肽释放酶排泄的变化与各种刺激后肾素 - 血管紧张素 - 醛固酮系统的变化有关，提示肾激肽释放酶 - 激肽系统可能通过对抗肾素 - 血管紧张素 - 醛固酮系统的作用来调节血压。尽管肾素 - 血管紧张素 - 醛固酮系统增强，但钠耗竭后尿PGE排泄减少，服用呋塞米后尿PGE排泄增加。各种刺激后尿PGE排泄的变化与尿钠排出的变化密切相关，并且尿PGE基础水平与尿钠基础水平之间存在显著正相关，提示肾前列腺素E可能通过影响肾钠处理参与血压调节。目前的数据表明，原发性高血压患者尿PGE和激肽释放酶的基础排泄水平低于正常受试者，并且与正常受试者相比，原发性高血压患者服用呋塞米后肾激肽释放酶和PGE的释放也受到抑制，提示在这种疾病中存在针对肾素 - 血管紧张素 - 醛固酮系统的防御机制受损，导致钠潴留。
