C. Bellini et al., THE INFLUENCE OF SALT SENSITIVITY ON THE BLOOD-PRESSURE RESPONSE TO EXOGENOUS KALLIKREIN IN ESSENTIAL HYPERTENSIVE PATIENTS, Nephron, 65(1), 1993, pp. 28-35
In order to verify the influence of salt sensitivity on the blood pres
sure response to orally administered kallikrein, we evaluated the effi
cacy of glandular kallikrein (derived from porcine pancreas) in 28 ess
ential hypertensives (21 males and 9 females) aged between 40 and 62 y
ears. After a placebo run-in period, the patients were assigned to rec
eive oral kallikrein therapy (150 IU 3 times a day; n = 18 patients) o
r placebo (n = 10 patients) over a period of 8 days in a random double
-blind fashion. In the salt-resistant patients (n = 8), kallikrein adm
inistration did not modify blood.pressure levels. In the same group, n
atriuresis increased significantly after the treatment [from 94.51 +/-
10.76 to 111.65 +/- 23.19 mEq/24 h (mmol/24 h), p < 0.039]. In the sa
lt-sensitive patients (n = 10), blood pressure decreased with the kall
ikrein therapy (systolic: from 158.50 +/- 9.20 to 144.50 +/- 10.12 mm
Hg, p < 0.005; diastolic: from 99.50 +/- 2.16 to 90.0 +/- 3.67 mm Hg,
p < 0.024). In the same patients, urinary Na+ excretion increased cons
iderably after the kallikrein treatment (from 101.07 +/- 18.36 to 134.
34 +/- 18.27 mEq/24 h, p < 0.0001). Therefore, our data indicate that
the oral kallikrein administration reduces blood pressure levels only
in the salt-sensitive hypertensives. In both the salt-sensitive and th
e salt-resistant groups a marked increase in the 24-hour urinary excre
tion of sodium was observed after the kallikrein treatment. Therefore,
the enhanced antihypertensive efficacy of the oral kallikrein adminis
tration observed in the sodium-sensitive patients is not only due to i
ts natriuretic action but also to different kallikrein-related effects
.