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首页> 美国卫生研究院文献>other >Candesartan Differentially Regulates Epithelial Sodium Channel in Cortex Versus Medulla of Streptozotocin-Induced Diabetic Rats
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Candesartan Differentially Regulates Epithelial Sodium Channel in Cortex Versus Medulla of Streptozotocin-Induced Diabetic Rats

机译：坎地沙坦差异调节链脲佐菌素诱导的糖尿病大鼠皮质与髓质的上皮钠通道。

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Diabetes is associated with an activated renal renin-angiotensin-aldosterone system (RAAS) and it was shown that streptozotocin (STZ)-induced diabetic rats had increased whole kidney protein levels of the epithelial sodium channel subunits (α-, β- and γ-ENaC). However, the role of the RAAS on the regional, i.e., cortical versus medullary, regulation of ENaC is unclear. Male Sprague-Dawley rats were injected with STZ (intravenous, 65 mg/kg·bw, n=12/group). After 14 days, half of them received drinking water with candesartan (2 mg/kg·bw/day), an angiotensin-II type-1 receptor (AT1R) antagonist, for one week. In the medulla, i.e., inner stripe of the outer medulla (ISOM), base and/or tip of the inner medulla, immunoblotting revealed increased protein abundances of α1 Na-K-ATPase and ENaC subunits with diabetes (200–600% of controls), which were not reversed by candesartan. In fact, candesartan increased all ENaC subunits and α1 Na-K-ATPase in the ISOM and/or base in control rats. In contrast, in the cortex, diabetes did not increase these proteins. However, candesartan reduced cortical β- and γ-ENaC regardless of diabetic state. In summary, diabetes-induced increases in ENaC were seen preferentially in the medulla. These changes appeared to be due to a mechanism clearly distinct from AT1R activation, because they were not abolished by candesartan. In fact, candesartan treatment tended to increase some of these medullary proteins, perhaps in compensation for increased NaCl load. In contrast, cortical β- and γ-ENaC were reduced by candesartan regardless of diabetic state suggesting their regulation by AT1R at this site; however this did not appear to be a site of diabetes-induced ENaC up-regulation.
机译：糖尿病与激活的肾素-血管紧张素-醛固酮系统（RAAS）相关，并且显示链脲佐菌素（STZ）诱导的糖尿病大鼠上皮钠通道亚基（α-，β-和γ- ENaC）。然而，尚不清楚RA​​AS在ENaC的区域调节中的作用，即皮质调节与髓样调节。雄性Sprague-Dawley大鼠注射STZ（静脉注射，剂量65 mg / kg·bw，n = 12 /组）。 14天后，其中一半的人接受了坎地沙坦（2 mg / kg·bw /天）的饮用水，这是一种血管紧张素II型1受体（AT1R）拮抗剂。在延髓（即延髓的内条纹（ISOM），延髓的基部和/或尖端）中，免疫印迹显示糖尿病患者中α1Na-K-ATPase和ENaC亚基的蛋白质丰度增加（对照组的200–600％ ），而坎地沙坦并没有逆转。实际上，坎地沙坦可增加对照组大鼠ISOM和/或碱基中的所有ENaC亚基和α1Na-K-ATPase。相反，在皮质中，糖尿病并未增加这些蛋白质。但是，坎地沙坦可降低皮质β-和γ-ENaC，而与糖尿病状态无关。总之，优先在延髓中观察到糖尿病引起的ENaC升高。这些变化似乎是由于明显不同于AT1R激活的机制所致，因为坎地沙坦并未消除它们。实际上，坎地沙坦治疗可能会增加其中一些髓质蛋白，也许是为了补偿NaCl的增加。相反，坎地沙坦可降低皮质β-和γ-ENaC的表达，而与糖尿病状态无关，表明它们在该部位受AT1R调节。但是，这似乎不是糖尿病引起的ENaC上调的部位。

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