Ideishi M, Miura S, Sakai T, Sasaguri M, Misumi Y, Arakawa K
Department of Internal Medicine, Fukuoka University School of Medicine, Japan.
J Hypertens. 1994 Jun;12(6):653-61.
To determine whether taurine reduces blood pressure by stimulating the renal kallikrein-kinin system.
The effects of taurine on blood pressure, urinary kallikrein activity and renal kallikrein gene expression were investigated in Dahl salt-sensitive (Dahl-S) rats. The specificity of the action of taurine was verified by comparison with the action of beta-alanine, a carboxylic analogue of taurine. The effect of co-administration of the specific bradykinin B2 receptor antagonist Hoe 140 was also examined.
Administration of taurine (3% in drinking water) for 4 weeks retarded the development of salt (4% sodium chloride diet)-induced hypertension. Systolic blood pressure at the end of the experiment was significantly higher in control rats than in taurine-treated rats. Urinary sodium excretion was not decreased by the reduction in blood pressure. The heart weight:body weight ratio was significantly lower, and urinary volume and kallikrein excretion were significantly higher, in taurine-treated rats. Renal kallikrein gene expression at weeks 1 and 4 was higher in taurine-treated rats. Systolic blood pressure 3 and 4 weeks after the administration of beta-alanine was slightly, but not significantly, lower than that of untreated rats on a high-salt diet, and was accompanied by a significantly lower body weight. Urinary kallikrein excretion decreased with a high-salt diet regardless of beta-alanine administration. Continuous systemic administration of Hoe 140 did not cause any significant alteration in blood pressure in Dahl-S rats that received taurine with a high-salt diet. Taurine also showed a renoprotective effect, as judged by a reduction in proteinuria.
These results suggest that taurine is an effective antihypertensive agent for salt-induced hypertension. Although taurine activated renal kallikrein, further studies are required to confirm the participation of activated kallikrein in the antihypertensive, cardioprotective and renoprotective effects of taurine.
确定牛磺酸是否通过刺激肾激肽释放酶-激肽系统来降低血压。
在 Dahl 盐敏感（Dahl-S）大鼠中研究了牛磺酸对血压、尿激肽释放酶活性和肾激肽释放酶基因表达的影响。通过与牛磺酸的羧酸类似物β-丙氨酸的作用进行比较，验证了牛磺酸作用的特异性。还检查了联合给予特异性缓激肽 B2 受体拮抗剂 Hoe 140 的效果。
给予牛磺酸（饮用水中含 3%）4 周可延缓盐（4%氯化钠饮食）诱导的高血压的发展。实验结束时，对照大鼠的收缩压显著高于牛磺酸处理的大鼠。血压降低并未使尿钠排泄减少。牛磺酸处理的大鼠的心脏重量与体重之比显著更低，尿量和激肽释放酶排泄显著更高。牛磺酸处理的大鼠在第 1 周和第 4 周时肾激肽释放酶基因表达更高。给予β-丙氨酸 3 周和 4 周后的收缩压略低于高盐饮食未处理大鼠，但差异不显著，且体重显著更低。无论是否给予β-丙氨酸，高盐饮食都会使尿激肽释放酶排泄减少。在接受高盐饮食牛磺酸的 Dahl-S 大鼠中，持续全身给予 Hoe 140 并未引起血压的任何显著变化。从蛋白尿减少判断，牛磺酸还显示出肾脏保护作用。
这些结果表明，牛磺酸是盐诱导高血压的有效抗高血压药物。尽管牛磺酸激活了肾激肽释放酶，但需要进一步研究来证实激活的激肽释放酶参与了牛磺酸的抗高血压、心脏保护和肾脏保护作用。
