The renin-angiotensin system plays a role in the pathophysiology of
renovascular hypertension. In addition, some studies have demonstrated a beneficial effect of
L-arginine (L-Arg), the precursor of
nitric oxide (NO), in this model of
hypertension. This study was designed to investigate the effects of L-Arg on cardiovascular parameters and on the activity of the
angiotensin-converting enzyme (ACE), after 14 days of
renovascular hypertension. The experiments were performed on conscious male Wistar rats. Two-kidney, one-
clip renovascular hypertension (2KIC) was initiated in rats by clipping the left renal artery during 14 days, while control rats were
sham-operated. One group was submitted to a similar procedure and treated with L-Arg (10 mg/ml; average intake of 300mg/day) from the 7th to the 14th day after surgery, whereas the respective control group received water instead. At the end of the treatment period, the mean arterial pressure (MAP) was measured in conscious animals. The rats were sacrificed and the ACE activity was assayed in heart and kidneys, using
Hip-His-Leu as substrate. In a separate group, the heart was removed, the left ventricle (LV) was weighed and the LV/
body weight ratios (LV/BW) were determined. We observed significant differences in MAP between the L-Arg-treated and untreated groups (129 +/- 7 vs. 168 +/- 6 mmHg; P< 0.01). The
cardiac hypertrophy described for this model of
hypertension was attenuated in the 2K1C-L-Arg-treated group (14th day, wet LV/BW: 2K1C-L-Arg = 1.88 +/- 0.1; 2K1C = 2.20 +/- 0.1 mg/g; P < 0.05). L-Arg administration caused an important decrease in cardiac ACE activity (2K1C-L-Arg: 118 +/- 15; 2K1C: 266 +/- 34 micromol/min/mg; P < 0.01). L-Arg also decreased the ACE activity in the clipped kidney by 47% (P < 0.01), but not in the nonclipped kidney. These data suggest that increased NO formation and reduced
angiotensin II formation are involved in the anthihypertensive effect of orally administered
L-arginine.