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首页> 外文期刊>American Journal of Physiology >Salt-sensitive hypertension develops after transient induction of ANG II-dependent hypertension in Cyp1a1-Ren2 transgenic rats.
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Salt-sensitive hypertension develops after transient induction of ANG II-dependent hypertension in Cyp1a1-Ren2 transgenic rats.

机译：在Cyp1a1-Ren2转基因大鼠中短暂诱导ANG II依赖性高血压后，就会出现盐敏感性高血压。

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Transient exposure to ANG II results in the development of salt-sensitive hypertension in rats. This study was performed to determine whether a transient hypertensive episode can induce salt-sensitive hypertension in transgenic rats with inducible expression of the mouse Ren2 renin gene [strain name TGR(Cyp1a1-Ren2)]. Systolic blood pressures were measured in conscious male Cyp1a1-Ren2 rats (n = 6) during control conditions and during dietary administration of indole-3-carbinol (I3C; 0.15%, wt/wt), for 14 days. Systolic pressure increased from 135 +/- 5 to 233 +/- 7 mmHg by day 14. I3C administration was terminated and blood pressure returned to normal levels (137 +/- 5 mmHg) within 10 days. Subsequently, the rats were placed on a high-salt diet (8% NaCl) for 10 days. Systolic pressure increased by 34 +/- 2 mmHg throughout 10 days of the high-salt diet. Neither glomerular filtration rate nor renal plasma flow was altered in Cyp1a1-Ren2 rats with salt-sensitive hypertension. In a separate group of male Cyp1a1-Ren2 rats (n = 6) transiently induced with 0.15% I3C for 14 days, administration of the superoxide dismutase mimetic tempol (4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl, 2 mM) attenuated the increase in systolic pressure induced by high salt. Systolic pressure increased by only 11 +/- 1 mmHg throughout 8 days of a high-salt diet and tempol administration. Thus transient induction of ANG II-dependent hypertension via activation of the Cyp1a1-Ren2 transgene induces salt-sensitive hypertension in these transgenic rats. The attenuation by tempol of the high salt-induced blood pressure elevation indicates that ANG II-induced production of superoxide anion contributes to the development of salt-sensitive hypertension after transient induction of ANG II-dependent hypertension.
机译：短暂暴露于ANG II会导致大鼠发生盐敏感性高血压。进行这项研究是为了确定短暂性高血压发作是否可以在可诱导表达小鼠Ren2肾素基因[菌株名称TGR（Cyp1a1-Ren2）]的转基因大鼠中诱发盐敏感性高血压。在控制条件下和吲哚-3-甲醇（I3C; 0.15％，wt / wt）的饮食管理下，连续14天在有意识的雄性Cyp1a1-Ren2大鼠（n = 6）中测量收缩压。到第14天，收缩压从135 +/- 5 mmHg增加到233 +/- 7 mmHg。终止I3C给药，并且在10天内血压恢复到正常水平（137 +/- 5 mmHg）。随后，将大鼠置于高盐饮食（8％NaCl）中10天。在高盐饮食的10天内，收缩压增加了34 +/- 2 mmHg。 Cyp1a1-Ren2盐敏感性高血压大鼠的肾小球滤过率和肾血浆流量均未改变。在另一组雄性Cyp1a1-Ren2大鼠（n = 6）中，用0.15％I3C瞬时诱导14天，施用超氧化物歧化酶模拟tempol（4-羟基-2,2,6,6-四甲基哌啶氧基，2 mM ）减轻了高盐引起的收缩压升高。在高盐饮食和服用tempol的8天中，收缩压仅增加11 +/- 1 mmHg。因此，通过激活Cyp1a1-Ren2转基因短暂诱导ANG II依赖性高血压会在这些转基因大鼠中诱导盐敏感性高血压。 tempol对高盐诱导的血压升高的衰减表明，在短暂诱导ANG II依赖性高血压后，ANG II诱导的超氧阴离子的产生有助于盐敏感性高血压的发展。

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