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首页> 外文期刊>American Journal of Physiology >Downregulation of nitric oxide synthase in chronic renal insufficiency: role of excess PTH.
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Downregulation of nitric oxide synthase in chronic renal insufficiency: role of excess PTH.

机译：一氧化氮合酶在慢性肾功能不全中的下调：过量PTH的作用。

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The available data on the effect of chronic renal failure (CRF) on nitric oxide (NO) metabolism are limited and contradictory. We studied rats with CRF 6 wk after a five-sixths nephrectomy and compared the results with those in the sham-operated controls, felodipine-treated CRF, and parathyroidectomized (CRF-PTX) animals. CRF was produced by surgical resection of the upper and lower thirds of the left kidney, followed by contralateral nephrectomy. We chose this model, as opposed to that produced by renal artery branch ligation, because the latter causes exuberant hypertension (HTN), which independently affects NO metabolism. The CRF group exhibited a mild HTN coupled with elevated basal platelet cytosolic Ca2+ concentration ([Ca2+]i), blunted hypotensive response to L-arginine, decreased hypertensive response to NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine, and normal hypotensive response to NO donor, sodium nitroprusside. This was associated with a significant reduction in urinary excretion of stable NO metabolites (NOX) and depressed NOS activity, as well as endothelial and inducible NO synthase (eNOS and iNOS, respectively) protein contents of thoracic aorta and the remnant kidney in the CRF animals. Calcium channel blockade and PTX lowered blood pressure, increased urinary NOX, and enhanced vascular NOS activity, as well as eNOS and iNOS protein expressions in the tested tissues. Thus CRF animals exhibited significant reductions in vascular NOS activity and eNOS and iNOS expressions. These abnormalities were reversed by calcium channel blockade and PTX, suggesting the possible causal role of CRF-induced dysregulation of [Ca2+]i.
机译：关于慢性肾功能衰竭（CRF）对一氧化氮（NO）代谢的影响的可用数据有限且相互矛盾。我们研究了六分之五的肾切除术后6周CRF的大鼠，并将结果与​​假手术对照组，非洛地平治疗的CRF和甲状旁腺切除术（CRF-PTX）的动物进行了比较。 CRF是通过手术切除左肾的上部和下部三分之二，然后进行对侧肾切除术而产生的。我们选择这种模型，而不是通过肾动脉分支结扎产生模型，因为后者会引起旺盛的高血压（HTN），独立影响NO代谢。 CRF组表现为轻度HTN，伴有基础血小板胞浆Ca2 +浓度（[Ca2 +] i）升高，对L-精氨酸的低血压反应减弱，对NO合酶（NOS）抑制剂，NG-单甲基-L-精氨酸的高血压反应降低，以及对NO供体硝普钠的正常降压反应。这与CRF动物中稳定的NO代谢物（NOX）的尿排泄和NOS活性降低以及胸主动脉和残余肾脏的内皮和诱导型NO合酶（分别为eNOS和iNOS）蛋白质含量显着降低有关。 。钙通道阻滞和PTX降低了血压，增加了尿中的NOX并增强了血管NOS活性以及被测组织中的eNOS和iNOS蛋白表达。因此，CRF动物表现出血管NOS活性以及eNOS和iNOS表达的显着降低。钙通道阻滞和PTX逆转了这些异常，提示CRF诱导的[Ca2 +] i失调可能是因果关系。

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