Mehta S, Stewart D J, Levy R D
Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
Chest. 1996 Jun;109(6):1550-5. doi: 10.1378/chest.109.6.1550.
Endothelial metabolism of L-arginine to L-citrulline and the potent vasodilator, nitric oxide (NO), is important in the regulation of vascular tone and resting BP. L-arginine improves abnormal endothelium-dependent vasodilation in the setting of hypercholesterolemia and has a vasodilatory effect in normal vessels, effects presumed to be mediated through increased endogenous NO production, although this has not been established by direct measurement of NO. In a randomized, placebo-controlled, crossover trial, 10 healthy male subjects received a 30-min infusion of 0.5 g/kg L-arginine hydrochloride. Subjects underwent continuous monitoring of BP and heart rate (HR) as well as intermittent determination of mixed expired NO concentration and plasma L-arginine and L-citrulline levels. Infusion of L-arginine produced a significant fall in mean BP with a peak effect of -9.3 +/- 0.9% (p<0.005). The hemodynamic effects of L-arginine were associated with an increase in mixed expired NO concentration (FeNO) of 55 +/- 15% (p<0.005) from 15 +/- 2 to 21 +/- 3 parts per billion (ppb) and an increase in the rate of pulmonary NO excretion of 118 +/- 45% (p<0.005), as well as a rise in plasma L-citrulline from 25 +/- 4 to 46 +/- 5 micromol/l (p<0.005). There was a significant correlation between the hypotensive response to L-arginine and the increase in expired NO (r=-0.68, p<0.05). The hypotensive effect of L-arginine in humans appears to be mediated, at least in part, by NO synthase metabolism of L-arginine and increased endogenous NO production as indicated both by increased plasma L-citrulline and by increased expired NO.
内皮细胞将L-精氨酸代谢为L-瓜氨酸和强效血管舒张剂一氧化氮（NO），这在调节血管张力和静息血压方面具有重要作用。L-精氨酸可改善高胆固醇血症情况下异常的内皮依赖性血管舒张，并对正常血管具有血管舒张作用，这些作用推测是通过增加内源性NO生成来介导的，尽管尚未通过直接测量NO来证实这一点。在一项随机、安慰剂对照的交叉试验中，10名健康男性受试者接受了30分钟的0.5 g/kg盐酸L-精氨酸输注。受试者接受了血压和心率（HR）的连续监测，以及混合呼出NO浓度、血浆L-精氨酸和L-瓜氨酸水平的间歇性测定。输注L-精氨酸导致平均血压显著下降，峰值效应为-9.3±0.9%（p<0.005）。L-精氨酸的血流动力学效应与混合呼出NO浓度（FeNO）从15±2 ppb增加到21±3 ppb（增加55±15%，p<0.005）、肺NO排泄率增加118±45%（p<0.005）以及血浆L-瓜氨酸从25±4 μmol/l升高到46±5 μmol/l（p<0.005）有关。对L-精氨酸的降压反应与呼出NO增加之间存在显著相关性（r=-0.68，p<0.05）。L-精氨酸在人体中的降压作用似乎至少部分是由L-精氨酸的NO合酶代谢和内源性NO生成增加介导的，这一点通过血浆L-瓜氨酸增加和呼出NO增加均得到了证实。
