ヒト尿中 Prekallikrein に関する研究 ―測定法の確立と本態性及び内分泌性高血圧症におけるその臨床応用―

概要

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In order to clarify the pathophysiological role of renal kallikrein-kinin system, a new method for the measurement of urinary prekallikrein was established, and urinary excretions of total kallikrein, kallikrein and prekallikrein were determined in the patients with essential hypertension, primary aldosteronism and Cushing syndrome. Urinary prekallikrein was converted to an active form by trypsin treatment. Urinary total kallikrein was determined by measuring the kallikrein levels after trypsin treatment. Urinary prekallikrein levels were calculated by subtracting active kallikrein values from total kallikrein values. Kallikrein was measured by both the direct radioimmunoassay (enzyme quantity) and kininogenase assay (enzyme activity) methods. Significant correlations were obtained between immunoreactive kallikrein and kininogenase activity in total kallikrein, active kallikrein and prekallikrein. In essential hypertensives,urinary excretion of total kallikrein which reflects the renal prekallikrein synthesis, was significantly lower than that in normal subjects. The same tendency was also observed in the urinary excretion of active kallikrein. However, urinary kallikrein/total kallikrein ratio reflecting the conversion ratio from prekallikrein to an active form in the kidney, was the same as normal subjects. These data suggest that the suppressed urinary kallikrein excretion in essential hypertensive patients, may be explained mainly by the inhibited synthesis of prekallikrein in the kidney, and not by a disturbance of the conversion process from prekallikrein to an active form. In the patients with primary aldosteronism, urinary excretion of kallikrein, total kallikrein and conversion ratio from prekallikrein to an active form were significantly higher than those in normal subjects, suggesting that the augmented urinary excretion of kallikrein in the patients with primary aldosteronism, may be caused by an increase of both the prekallikrein synthesis and conversion from prekallikrein to an active form. In the patients with Cushing syndrome, urinary excretion of total kallikrein and active kallikrein showed no significant differences from those of normal subjects. However, the conversion ratio from a prekallikrein to an active one increased significantly compared to that of normal subjects. The mechanism of the increase in the conversion ratio for Cushing syndrome still remains unknown, although the glucocorticoid may be connected with this mechanism. Thus, it was concluded that the determination of all components of renal kallikrein-kinin system including prekallikrein seems to be useful to investigate the pathophysiological role of renal kallikrein-kinin system in various hypertensive diseases.
札幌医科大学の論文
1987-12-01

ヒト尿中 Prekallikrein に関する研究 ―測定法の確立と本態性及び内分泌性高血圧症におけるその臨床応用―

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札幌医科大学 | 論文

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