Franchi F, Lo Sapio P, Strazzulla G, Fabbri G, Scardi A, Pinzani M, Laffi G, Mannelli M
Int J Clin Pharmacol Ther Toxicol. 1987 Jan;25(1):44-9.
The activity of basal 24-hour urinary kallikrein activity (UKA), prostaglandin E2 (U. PGE2) and thromboxane B2 (U. TxB2) and their relationship to natriuresis (U. Sodium), urinary aldosterone (U. Aldosterone) and plasma renin activity (in supine position: PRA1; in standing position: PRA2) were evaluated in 20 patients with early-moderate hemodynamically defined (first pass and gate blood pool radionuclide angiocardiography) essential hypertension (H) and in 13 age-matched normotensive patients (N). In basal conditions, UKA and PRA2 were significantly reduced (p less than 0.005 and p less than 0.05, respectively) in H compared with N. However, no differences between N and H were found for U. TxB2, U. PGE2, U. Aldosterone, U. Sodium, and PRA1. All parameters were also evaluated both in H and N before and after the administration of furosemide (40 mg i.v.). In H, but not in N, furosemide induced an increase of UKA (p less than 0.05), U. TxB2 (p less than 0.05) and U. Sodium (p less than 0.001). In both H and N furosemide caused a significant rise of PRA1 (p less than 0.001 in H and p less than 0.01 in N) and PRA2 (p less than 0.001 in H and p less than 0.05 in N). In H a significant correlation was found between percent increases of U. Sodium and U. Kallikrein (r = 0.54, p less than 0.01) and between percent differences of PGE2 and TxB2 (r = 0.59, p less than 0.01). It is proposed that reduction of basal UKA may be an early evidence of the first stages of hypertension, i.e., in absence of renal and cardiovascular alteration. The finding is not accompanied by significant changes in urinary excretion of arachidonic acid metabolites and aldosterone. Finally, any relation between UKA values and systemic hemodynamics is lacking.
对20例早期 - 中度血流动力学定义（首次通过和门控血池放射性核素血管造影）的原发性高血压（H）患者和13例年龄匹配的血压正常患者（N），评估了基础24小时尿激肽释放酶活性（UKA）、前列腺素E2（U. PGE2）和血栓素B2（U. TxB2）的活性，以及它们与尿钠排泄（U. Sodium）、尿醛固酮（U. Aldosterone）和血浆肾素活性（仰卧位：PRA1；站立位：PRA2）的关系。在基础条件下，与N组相比，H组的UKA和PRA2显著降低（分别为p < 0.005和p < 0.05）。然而，在U. TxB2、U. PGE2、U. Aldosterone、U. Sodium和PRA1方面，N组和H组之间未发现差异。在H组和N组中，还在静脉注射速尿（40 mg）前后评估了所有参数。在H组而非N组中，速尿导致UKA（p < 0.05）、U. TxB2（p < 0.05）和U. Sodium（p < 0.001）增加。在H组和N组中，速尿均导致PRA1（H组p < 0.001，N组p < 0.01）和PRA2（H组p < 0.001，N组p < 0.05）显著升高。在H组中，发现U. Sodium的百分比增加与U. Kallikrein之间存在显著相关性（r = 0.54，p < 0.01），PGE2和TxB2的百分比差异之间也存在显著相关性（r = 0.59，p < 0.01）。有人提出，基础UKA的降低可能是高血压早期阶段的早期证据，即在没有肾脏和心血管改变的情况下。这一发现并未伴有花生四烯酸代谢产物和醛固酮尿排泄的显著变化。最后，UKA值与全身血流动力学之间不存在任何关系。
