Hypertension, Vol 5, 244-256, Copyright © 1983 by American Heart Association
FH Derkx, L Tan-Tjiong, GJ Wenting, F Boomsma, AJ Man in 't Veld and MA Schalekamp
An assay of plasma prorenin was developed in which the conversion to renin
occurred under apparently optimal conditions. Some characteristics of the
assay were 1) prorenin was activated by Sepharose-bound trypsin at 4
degrees C; 2) the concentration of activator was not critical provided that
incubation was prolonged until renin activity had reached a plateau; and 3)
this plateau was stable and had the same height as after maximal activation
with acid, pepsin, plasmin or urokinase. Maximal activity with
Sepharose-bound trypsin at 4 degrees C was higher than with cryoactivation,
and optimal conditions were more readily reproduced than with trypsin at 37
degrees C or with acid-activation. The assay was used for measurements in
peripheral and renal vein plasma after captopril in hypertensive patients
with unilateral renal artery stenosis. Peripheral renin rose within 30
minutes after a first dose of captopril, 50 mg orally, and it remained high
with chronic treatment. In contrast, peripheral prorenin fell initially and
rose after 4 hours. These changes in peripheral plasma were related to
changes in the secretion rates of the two forms of renin from the affected
kidney. Thus chronic, but not acute, stimulation of renin release was
associated with an increased secretion rate of prorenin. The late rise in
prorenin is probably an indication of enhanced synthesis in the kidney, so
that more prorenin is available for conversion. The data suggest that
prorenin is indeed a biosynthetic precursor of renin and that, at least
under certain circumstances, a major proportion of circulating prorenin
originates from the kidney.
ARTICLES
Asynchronous changes in prorenin and renin secretion after captopril in patients with renal artery stenosis
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