Y. Higashi et al., INTRAVENOUS ADMINISTRATION OF L-ARGININE INHIBITS ANGIOTENSIN-CONVERTING ENZYME IN HUMANS, The Journal of clinical endocrinology and metabolism, 80(7), 1995, pp. 2198-2202
The iv administration of L-arginine, a precursor of endothelium-derive
d relaxing factor/nitric oxide, is known to decrease blood pressure in
humans by its direct vasodilatory effects. The purpose of the present
study was to determine whether L-arginine infusion modifies the renin
-angiotensin (Ang)-aldosterone system as well as blood pressure and re
nal hemodynamics. L-Arginine and saline vehicle were iv administered t
o 10 healthy male subjects in random order on different days. L-Argini
ne infusion (500 mg/kg over 30 min) decreased mean blood pressure (fro
m 81.2 +/- 2,7 to 74.0 +/- 2.5 mm Hg; P < 0.001) and renal vascular re
sistance (from 0.085 +/- 0.007 to 0.074 +/- 0.306 mm Hg/mL . min; P <
0.01) and increased heart rate (from 60.3 +/- 2.7 to 69.7 +/- 2.1 beat
s/min; P < 0.001) and renal plasma flow (fr om 616.6 +/- 37.8 to 701.0
+/- 49,2 mL/min; P < 0.05). L-Arginine reduced serum Ang-converting e
nzyme acti;vity (from 10.4 +/- 0.6 to 8.9 +/- 0.5 nmol/mL . min; P < 0
.05) and plasma Ang-II (from 19.3 +/- 3.3 to 12.7 +/- 2.8 pg/mL; P < 0
.001), but had no effect on PRA or the glomerular filtration rate. The
saline vehicle did not alter any of these parameters. The iv administ
ration of L-arginine (endothelium-derived relaxing factor/nitric oxide
) may reduce the plasma Ang-II concentration by inhibiting Ang-convert
ing enzyme. The mechanism by which L-arginine infusion decreases blood
pressure can be at least in part explained by inhibition of the renin
-Ang system.