Hypertension, Vol 5, 603-609, Copyright © 1983 by American Heart Association
W Lieberthal, L Arbeit, NB Oza, DB Bernard and NG Levinsky
Urinary kallikrein excretion was studied in 34 patients with mild,
normal-renin, essential hypertension without evidence of target organ
damage and in 23 normotensive controls, using assays that measure both
active (kininogenase activity) and total (active plus inactive) kallikrein.
There was no significant difference in either active or total kallikrein
excretion between the two groups. However, the ratio of active-to-total
enzyme was decreased in the hypertensives (0.83 +/- 0.03 units/micrograms)
compared to the normotensives (1.00 +/- 0.05 units/micrograms) (p less than
0.002). The active-to-total ratio was inversely related to sodium excretion
in both groups, indicating that the proportion of active to inactive enzyme
increased in response to reduced sodium intake. We conclude that, although
absolute excretion of active and total kallikrein is not decreased, enzyme
activity per microgram of total kallikrein excreted is reduced in mild,
normal-renin essential hypertension. This abnormality may be due to a
defective enzyme, or to a reduced excretion of active relative to inactive
kallikrein. The latter could result from the presence of a urinary
kallikrein inhibitor or to reduced activation of a proenzyme.
ARTICLES
Reduced ratio of active-to-total urinary kallikrein in essential hypertension
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