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首页> 外文期刊>American Journal of Physiology >Posttranslational regulation of NO synthase activity in the renal medulla of diabetic rats.
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Posttranslational regulation of NO synthase activity in the renal medulla of diabetic rats.

机译：糖尿病大鼠肾延髓中NO合酶活性的翻译后调节。

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Shear stress increases nitric oxide (NO) production by endothelial cells, inner medullary collecting duct cells, and thick ascending limb. We postulated that the osmotic diuresis accompanying type 1 diabetes is associated with increased NO synthase (NOS) activity and/or expression in the renal medulla. Diabetes was induced by injection of streptozotocin, with insulin provided to maintain moderate hyperglycemia (Hyp) or euglycemia (Eug) for 3 wk. Sham rats received vehicle treatments. A separate group of rats (Phz) received phlorizin to produce a glucose-dependent osmotic diuresis. Renal medullary NOS1 and NOS2 activities did not differ between groups, whereas NOS3 activity was significantly increased in Hyp. Neither NOS1 nor NOS3 protein levels differed significantly between groups. Reduced phosphorylation of NOS3 at Thr(495) and Ser(633) was evident in medullary homogenates from Hyp rats, with no difference apparent at Ser(1177). Immunohistochemical analysis indicated prominent expression of pThr(495)NOS3 in the thick ascending limb and collecting duct of Sham and Phz rats. Hyp rats displayed staining in the collecting duct but minimal thick ascending limb staining. Immunostaining with anti-pSer(1177)NOS3 was evident only in the thick ascending limb, with no apparent differences between groups. In summary, glucose-dependent osmotic diuresis alone did not alter NOS activity or expression in the renal medulla. Diabetic hyperglycemia increased medullary NOS3 activity without a concomitant increase in NOS3 protein levels; however, NOS3 phosphorylation was reduced at Thr(495) and Ser(633). Thus changes in the phosphorylation of NOS at known regulatory sites might represent the primary mechanism underlying increased renal medullary NOS activity in diabetic hyperglycemia.
机译：剪切应力会增加内皮细胞，髓内收集导管细胞和上肢粗大上升产生的一氧化氮（NO）。我们假设伴随1型糖尿病的渗透性利尿与NO合酶（NOS）活性和/或肾髓质中表达的增加有关。糖尿病是通过注射链脲佐菌素诱导的，胰岛素可维持中度高血糖（Hyp）或正常血糖（Eug）3周。假大鼠接受载体治疗。另一组大鼠（Phz）接受phlorizin产生葡萄糖依赖性渗透性利尿剂。两组之间的肾脏髓质NOS1和NOS2活性没有差异，而Hyp明显增加了NOS3活性。两组之间的NOS1和NOS3蛋白水平均无显着差异。在Hyp大鼠的髓质匀浆中，在Thr（495）和Ser（633）处NOS3的磷酸化明显降低，而在Ser（1177）没有明显的差异。免疫组织化学分析表明，pThr（495）NOS3在Sham和Phz大鼠的厚上升肢和集气管中显着表达。 Hyp大鼠在收集管中显示出染色，但最小的上肢浓密染色。抗pSer（1177）NOS3的免疫染色仅在上升的粗肢中明显，两组之间无明显差异。总之，仅葡萄糖依赖性渗透性利尿剂不会改变肾脏髓质中的NOS活性或表达。糖尿病性高血糖增加了髓样NOS3的活性，而没有伴随NOS3蛋白水平的增加。但是，在Thr（495）和Ser（633）处NOS3磷酸化降低。因此，在已知的调节位点，NOS磷酸化的改变可能代表了糖尿病高血糖中肾髓质NOS活性增加的主要机制。

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