In vivo administration of -arginine: effects on blood pressure and vascular function in angiotensin II-induced hypertensive rats

Objective: We tested the hypothesis that -arginine ( -Arg), which is not a substrate for nitric oxide synthase but scavenges reactive oxygen in vitro, is protective in vivo. Methods: Rats were made hypertensive by administering angiotensin II (Ang II) (0.7 mg kg−1 per day) for 7 days (Ang II group). Two other groups additionally received either 3 mmol -Arg (Ang II + -Arg group) or vitamin C (1 g) (Ang II + Vit C group) per day. Sham-operated animals served as controls (n = 6–9). Systolic blood pressure was monitored daily and cardiovascular function determined ex vivo at 7 days. Results: Ang II raised systolic blood pressure to 184 mmHg, the increase was slightly attenuated by -Arg treatment (−17 mmHg; P< 0.05 versus Ang II alone) and prevented by Vit C. Acetylcholine-induced coronary relaxation was impaired in the Ang II group (P< 0.05 versus sham), the impairment was no different in the Ang II + -Arg group, but prevented by Vit C. Likewise, Vit C but not -Arg ameliorated reperfusion endothelium-dependent relaxation. However, in aortic rings -Arg slightly improved acetylcholine relaxation (P< 0.05). Oxidative stress load estimated in plasma with thiobarbituric acid reactive substance was higher in the Ang II than the sham group, Vit C abolished the increase, but -Arg was without effect. Conclusion: -Arg is weakly antihypertensive in vivo and ameliorates aortic, but not coronary endothelium-dependent relaxation ex vivo. Because -Arg had no effect on plasma oxidant status, this protection appears to be independent of reactive oxygen scavenging activity.