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首页> 外文期刊>American Journal of Physiology >Angiotensin II feedback is a regulator of renocortical renin, COX-2, and nNOS expression.
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Angiotensin II feedback is a regulator of renocortical renin, COX-2, and nNOS expression.

机译：血管紧张素II反馈是肾上腺皮质肾素，COX-2和nNOS表达的调节剂。

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Salt restriction leads to parallel increases of renin, cyclooxygenase-2 (COX-2), and neuronal nitric oxide synthase (nNOS) gene expression in the juxtaglomerular apparatus of rat kidneys. Because the upregulation of these genes is strongly enhanced if salt restriction is combined with inhibition of the renin-angiotensin-aldosterone system, our study aimed to find out whether the juxtaglomerular expressions of renin, COX-2, and nNOS are subject to a common direct negative feedback control by ANG II. For this purpose, male Sprague-Dawley rats were fed a low-salt diet (0.02% wt/wt) with or without additional treatment with the ANG I-converting enzyme (ACE) inhibitor ramipril (10 mg x kg body wt(-1) x day(-1)) for 1 wk, and renocortical renin, COX-2, and nNOS mRNAs were assayed. To narrow down possible indirect effects of the ACE inhibitor that may result from insufficient aldosterone production, the animals received mineralocorticoid substitution with fludrocortisone (6 mg. kg body wt(-1) x day(-1)). Thusmineralocorticoid substitution prevented the fall of systolic blood pressure and of glomerular filtration induced by ramipril in rats on low-salt diet. Although fludrocortisone had no effect on basal renin, COX-2, and nNOS mRNA, it clearly attenuated the threefold increases of both renin and COX-2 mRNA in response to low-salt diet. In rats on low-salt diet, ramipril further increased renin mRNA ninefold, COX-2 mRNA fourfold, and nNOS 2.5-fold in the absence of fludrocortisone. In the presence of fludrocortisone, ramipril increased renin mRNA 10-fold, COX-2 mRNA 2.5-fold, and nNOS mRNA 2.5-fold. These data indicate that mineralocorticoid substitution lowers the overall expression of juxtaglomerular renin and COX-2 during low-salt intake and attenuates a further rise of COX-2 expression by ACE inhibition, but it does not change the stimulatory effect of ACE inhibition on renin and nNOS expression. We conclude that the expression of renin, COX-2, and nNOS in the juxtaglomerular apparatus during low-salt diet is markedly limited by a direct feedback inhibition through ANG II.
机译：盐限制会导致大鼠肾小球旁器官中的肾素，环氧合酶2（COX-2）和神经元一氧化氮合酶（nNOS）基因表达平行增加。因为如果盐限制结合抑制肾素-血管紧张素-醛固酮系统，这些基因的上调会大大增强，所以我们的研究旨在确定肾素，COX-2和nNOS的近肾小管表达是否受共同的直接作用。 ANG II的负反馈控制。为了这个目的，雄性Sprague-Dawley大鼠接受低盐饮食（0.02％wt / wt），有或没有用ANG I转化酶（ACE）抑制剂雷米普利（10 mg x kg体重（-1） ）x天（-1））1周，测定肾上腺皮质肾素，COX-2和nNOS mRNA的表达。为了缩小由于醛固酮生产不足可能引起的ACE抑制剂的间接作用，动物接受了氟可的松（6 mg。kg体重（-1）x天（-1））的盐皮质激素替代。因此，盐皮质激素替代可防止低盐饮食大鼠中雷米普利引起的收缩压和肾小球滤过率下降。尽管氟氢可的松对基础肾素，COX-2和nNOS mRNA没有影响，但它明显减轻了低盐饮食对肾素和COX-2 mRNA的三倍增加。在低盐饮食的大鼠中，雷米普利在不存在氟可的松的情况下使肾素mRNA进一步增加9倍，COX-2 mRNA增加4倍，nNOS增加2.5倍。在氟氢可的松的存在下，雷米普利使肾素mRNA增加10倍，COX-2 mRNA增加2.5倍，nNOS mRNA增加2.5倍。这些数据表明盐皮质激素替代降低了低盐摄入过程中近肾小球肾素和COX-2的总体表达，并通过ACE抑制作用减弱了COX-2表达的进一步升高，但并没有改变ACE抑制作用对肾素和肾上腺素的刺激作用。 nNOS表达。我们得出的结论是，低盐饮食期间肾小球器官中肾素，COX-2和nNOS的表达明显受到ANG II直接反馈抑制的限制。

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