Hypertension, Vol 14, 375-378, Copyright © 1989 by American Heart Association
Mechanisms of suppression of renal kallikrein activity in low renin essential hypertension and renoparenchymal hypertension
K Shimamoto, A Masuda, T Ando, N Ura, M Nakagawa, Y Mori, H Nakagawa, T Sakakibara, H Ogata and O Iimura
Second Department of Internal Medicine, Sapporo Medical College, Japan.
The mechanism of suppression of renal kallikrein activity in low renin
essential hypertensive and renoparenchymal hypertensive patients was
investigated in this study. From Sephadex G-200 column chromatography
studies, a single kallikrein peak was observed in both kallikrein
radioimmunoassay and kininogenase activity in all samples from normal
subjects, low renin essential hypertensive and renoparenchymal hypertensive
patients, and in purified kallikrein solution. The enzyme- specific
activity around the kallikrein peak in all urine samples from each group
was significantly lower than that in purified kallikrein, and a
significantly lower specific activity was found in both patient groups than
was found in normal subjects. Moreover, it was also recognized that the
specific activity of kallikrein decreased in all cases with the increase of
the molecular weight of kallikrein, and this tendency was observed more
obviously in the low renin essential hypertensive and renoparenchymal
hypertensive patients than in the normal subjects. These results suggest
the presence of a kallikrein- specific inhibitor with a low molecular
weight in human urine, although the possibility of a variant form of
kallikrein cannot be excluded.