The Excretion of Human Urinary Kallikrein Quantity and Activity in Normal and Low Renin Subgroups of Essential Hypertension

Abstract

In both low and normal renin essential hypertensive groups, urinary excretion of kallikrein quantity by direct radioimmunoassay and activity by kininogenase assay were significantly lower than those in normal subjects. In comparing between normal and low renin groups, no difference was found in kallikrein quantity, while kallikrein activity tended to be lower in the low renin group than in the normal renin group. A significant positive correlation was observed between kallikrein quantity and activity in the normal subjects, the normal renin group and the low renin group. However, the slope of the regression line in the low renin group was significantly more moderate than that in the normal renin group, and tended to be more moderate than that in normal subjects. The addition of kallikrein inhibitors (aprotinin and gabexate mesilate) resulted in a significant suppression of enzymatic activity but not of enzyme quantity. These findings suggest that suppression of the renal kallikrein system in both groups of essential hypertension was confirmed by the decreased excretion of kallikrein both as enzyme quantity and activity, and that in the mechanism of the suppression of urinary kallikrein activity in the low renin group, the renal kallikrein inhibitors may play some role.

Molecular Genetic Analyses of RFLPs for PCR-Amplified Growth Hormone Gene, Renal Kallikrein Gene and Atrial Natriuretic Factor Gene in Essential Hypertension.

“…Each of these functions are performed by renal kallikrein (13) and atrial natriuretic factor (ANF) (14), so that involvement of their respective genes in HT merits investigation. Early reports of reduced kallikrein excretion (15,16) have been confirmed in many studies (reviewed in 13) and appear to be most marked in low renin HT (17) . Even normal values in HT (13) might be deemed inappropriate.…”

Effect of metoprolol on 24‐hour urinary excretion of adrenal steroids and kallikrein in patients with essential hypertension

“…There are several known interrelationships between the kallikrein and the renin systems: these include the activation of prekallikrein and prorenin by serine proteases such as plasmin and the demonstration of the presence of prekallikrein, kallikrein, renin and converting enzyme of kininase II in the same membrane fraction of the distal tubular cells, suggesting interactions between hypertensive and hypotensive enzyme systems (Erdos & Yamada, 1982). Kallikrein activity tends also to be lower in low-renin hypertensives than in normal-renin patients and the slope of the regression line between urinary kallikrein quantity and activity has been reported to be significantly less steep in low-renin hypertensives (Ura et al, 1983), supporting a link between the renin and the kallikrein system also in chronic hypertension. The decrease in 24 h urinary aldosterone excretion after metoprolol along with a reduced kallikrein excretion, is consistent with earlier findings suggesting that mineralocorticoids may serve as the major link between the renin and the kallikrein systems.…”

The Influence of Salt Sensitivity on the Blood Pressure Response to Exogenous Kallikrein in Essential Hypertensive Patients

“…The association between a reduced urinary excretion of kallikrein and low renin activity has often been reported [20][21][22], and the presence of raised ANF levels in low-renin hypertensives has already been described [23].…”