It is believed that angiotensin converting-enzyme (ACE) inhibitors low
er proteinuria by acting on glomerular hemodynamics. This hypothesis p
redicts that the urinary excretion of a tubular protein should be unaf
fected by ACE inhibition, in the present study we have compared the ex
cretion of albumin and Tamm-Horsfall Glycoprotein (THGP), a protein se
creted only by renal tubules, before and after ACE inhibition. Urinary
protein excretion was measured with the Phast System, a method based
on SDS polyacrylamide gel electrophoresis followed by silver staining,
in 15 essential hypertensives, after at least 4 weeks of wash-out fro
m any drug and after 2 months of ACE inhibition with oral Quinapril. A
fter 2 months of ACE inhibition, blood pressure (BP), body weight, uri
nary output, heart rate, plasma glucose, plasma and urinary creatinine
, urate and electrolytes, and creatinine clearance, were not different
from baseline values. Plasma ACE activity decreased from 76 +/- 7 to
10 +/- 4 U/mL (mean +/- SEM, 2 tails paired t test, p = 0. 0001). Both
albumin and THP urinary excretions decreased from 51 +/- 6 to 43 +/-
4 mg/24 h (p = 0.05) and from 19 +/- 3 to 12 +/- 1 mg/24 h (p = 0.02),
respectively. This unexpected result suggests that ACE inhibitors may
act also at the level of renal tubular cells.