Mozaffari M S, Azuma J, Patel C, Schaffer S W
Department of Oral Biology/Pharmacology, Medical College of Georgia School of Dentistry, Augusta 30912-1128, U.S.A.
Biochem Pharmacol. 1997 Sep 1;54(5):619-24. doi: 10.1016/s0006-2952(97)00213-x.
Taurine is found in high concentrations in mammalian cells. Despite recognition of its role as an organic osmolyte in the kidney, information regarding its effects on renal fluid and electrolyte excretion is sparse. Therefore, the objective of the first series of experiments was to determine the effects of taurine depletion on renal excretory responses to a saline load. To induce taurine depletion, male Wistar-Kyoto (WKY) rats were treated with tap water containing 3% beta-alanine for 3 weeks. Taurine depletion reduced the initial rates of fluid and sodium excretion after an intravenous saline load. This effect was attributed to taurine depletion since maintenance of the taurine-depleted rats on tap water for 2 days to remove the effects of beta-alanine yielded the same pattern as the taurine-depleted rats exposed to beta-alanine at the time of the experiment. Nonetheless, rats exposed to short-term beta-alanine treatment, which has no influence on kidney taurine content, demonstrated a larger (approximately 25%) natriuretic but not diuretic response to the isotonic saline load than either the control or taurine-depleted rats. These data suggest that beta-alanine-induced inhibition of tubular reabsorption of taurine may result in subsequent excretion of taurine with attendant natriuresis early in the course of beta-alanine treatment. We also tested the hypothesis that taurine potentiates the renal excretory responses to an isotonic saline load in WKY rats. Inclusion of taurine in the infusate significantly increased natriuresis and diuresis after a saline load. This effect was greater in animals fed a basal than a high NaCl diet. Our data support a role for taurine as a natriuretic and diuretic agent.
牛磺酸在哺乳动物细胞中含量很高。尽管人们认识到它在肾脏中作为一种有机渗透质的作用,但关于其对肾液和电解质排泄影响的信息却很少。因此,第一系列实验的目的是确定牛磺酸耗竭对肾脏对盐水负荷排泄反应的影响。为了诱导牛磺酸耗竭,雄性Wistar-Kyoto(WKY)大鼠用含3%β-丙氨酸的自来水处理3周。牛磺酸耗竭降低了静脉注射盐水负荷后液体和钠的初始排泄率。这种效应归因于牛磺酸耗竭,因为让牛磺酸耗竭的大鼠在自来水中维持2天以消除β-丙氨酸的影响,其结果与实验时暴露于β-丙氨酸的牛磺酸耗竭大鼠相同。然而,接受短期β-丙氨酸处理(对肾脏牛磺酸含量无影响)的大鼠,对等渗盐水负荷的利尿钠反应比对照组或牛磺酸耗竭组大鼠更大(约25%),但无利尿反应。这些数据表明,β-丙氨酸诱导的肾小管对牛磺酸重吸收的抑制可能导致在β-丙氨酸处理早期牛磺酸随之排泄并伴有利尿钠作用。我们还测试了牛磺酸增强WKY大鼠对等渗盐水负荷肾排泄反应的假设。在输注液中加入牛磺酸可显著增加盐水负荷后的利尿钠和利尿作用。这种效应在喂食基础饮食的动物中比喂食高NaCl饮食的动物中更大。我们的数据支持牛磺酸作为一种利尿钠和利尿剂的作用。