Turner S W, Wen C, Li M, Whitworth J A
Department of Medicine, St George Hospital, University of New South Wales, Sydney, Australia.
Hypertension. 1996 Feb;27(2):184-9. doi: 10.1161/01.hyp.27.2.184.
In this study we examined whether L-arginine treatment could prevent corticotropin (ACTH)-induced increases in blood pressure in the Sprague-Dawley rat. Sixty rats were randomly divided into six groups (n = 10): sham injection, ACTH injection (0.5 mg/kg per day in divided doses), L-arginine (0.6%) in food plus sham injection, L-arginine plus ACTH treatment, D-arginine (0.6%) in food plus sham injection, and D-arginine plus ACTH. Systolic pressure, water intake, urine volume, body weight, plasma and urinary electrolytes, and serum corticosterone concentrations were measured. ACTH increased systolic pressure (from 127 +/- 2 to 165 +/- 6 mm Hg, P < .001), water intake, and urine volume and decreased body weight body weight. L-Arginine reduced ACTH-induced blood pressure rises (130 +/- 3 mm Hg, P < .001) but had no effect on blood pressure in sham-treated rats. D-Arginine did not affect blood pressure in sham-treated rats, and systolic pressure in D-arginine+ACTH-treated rats was similar to that of ACTH-treated rats. L-Arginine decreased serum corticosterone concentrations in sham-treated rats (424 +/- 42 versus 238 +/- 25 ng/mL, P < .01), but D-arginine had no effect. However, both drugs decreased serum corticosterone concentrations in ACTH-treated rats (1071 +/- 117 versus 739 +/- 95 and 695 +/- 72 ng/mL for L- and D-arginine, respectively; both P < .05). As L-arginine but not D-arginine prevented ACTH-induced increases in blood pressure in Sprague-Dawley rats and both L- and D-arginine reduced serum corticosterone concentrations in ACTH-treated rats, the effects of L-arginine in preventing ACTH-induced hypertension were not simply a consequence of decreased corticosterone secretion.
在本研究中，我们检测了L-精氨酸治疗是否能预防促肾上腺皮质激素（ACTH）诱导的斯普拉格-道利大鼠血压升高。60只大鼠被随机分为6组（每组n = 10）：假注射组、ACTH注射组（每天0.5 mg/kg，分剂量注射）、食物中含L-精氨酸（0.6%）加假注射组、L-精氨酸加ACTH治疗组、食物中含D-精氨酸（0.6%）加假注射组以及D-精氨酸加ACTH组。测量了收缩压、饮水量、尿量、体重、血浆和尿液电解质以及血清皮质酮浓度。ACTH使收缩压升高（从127±2 mmHg升至165±6 mmHg，P <.001），增加了饮水量和尿量，并降低了体重。L-精氨酸减轻了ACTH诱导的血压升高（130±3 mmHg，P <.001），但对假处理大鼠的血压无影响。D-精氨酸对假处理大鼠的血压无影响，D-精氨酸加ACTH处理大鼠的收缩压与ACTH处理大鼠相似。L-精氨酸降低了假处理大鼠的血清皮质酮浓度（424±42 ng/mL对238±25 ng/mL，P <.01），但D-精氨酸无此作用。然而，两种药物都降低了ACTH处理大鼠的血清皮质酮浓度（L-精氨酸和D-精氨酸分别为1071±117 ng/mL对739±95 ng/mL和695±72 ng/mL；两者P <.05）。由于L-精氨酸而非D-精氨酸预防了ACTH诱导的斯普拉格-道利大鼠血压升高，且L-精氨酸和D-精氨酸都降低了ACTH处理大鼠的血清皮质酮浓度，因此L-精氨酸预防ACTH诱导的高血压的作用并非仅仅是皮质酮分泌减少的结果。
