Role of the aldosterone-sensitive distal nephron in the sodium retention associated with liver cirrhosis

The renal mechanisms underlying sodium retention during liver cirrhosis have been difficult to elucidate. Kim and associates describe a biphasic pattern of regulation of the renal epithelial sodium channel in the common bile duct ligation model, shedding some light on this issue

17-β Estradiol attenuates streptozotocin-induced diabetes and regulates the expression of renal sodium transporters

Diabetes mellitus is associated with natriuresis, whereas estrogen has been shown to be renoprotective in diabetic nephropathy and may independently regulate renal sodium reabsorption. The aim of this study was to determine the effects of 17-β estradiol (E2) replacement to diabetic, ovariectomized (OVX) female rats on the expression of major renal sodium transporters. Female, Sprague–Dawley rats (210 g) were randomized into four groups: (1) OVX; (2) OVX+E2; (3) diabetic+ovariectomized (D+OVX); and (4) diabetic+ovariectomized+estrogen (D+OVX+E2). Diabetes was induced by a single intraperitoneal injection of streptozotocin (55 mg/kg·body weight (bw)). Rats received phytoestrogen-free diet and water ad libitum for 12 weeks. E2 attenuated hyperglycemia, hyperalbuminuria, and hyperaldosteronism in D rats, as well as the diabetes-induced changes in renal protein abundances for the bumetanide-sensitive Na–K–2Cl cotransporter (NKCC2), and the α- and β-subunits of the epithelial sodium channel (ENaC), that is, E2 decreased NKCC2, but increased α- and β-ENaC abundances. In nondiabetic rats, E2 decreased plasma K+ and increased urine K+/Na+ ratio, as well as decreased the abundance of NKCC2, β-ENaC, and α-1-Na–K–adenosine triphosphate (ATP)ase in the outer medulla. Finally, the diabetic, E2 rats had measurably lower final circulating levels of E2 than the nondiabetic E2 rats, despite an identical replacement protocol, suggesting a shorter biological half-life of E2 with diabetes. Therefore, E2 attenuated diabetes and preserved renal sodium handling and related transporter expression levels. In addition, E2 had diabetes-independent effects on renal electrolyte handling and associated proteins

Renal ENaC subunit, Na–K–2Cl and Na–Cl cotransporter abundances in aged, water-restricted F344 × Brown Norway rats

Renal sodium reabsorption is a key determinant of final urine concentration. Our aim was to determine whether differences existed between aged and young rats in their response to water restriction with regard to the regulation of abundance of any of the major distal renal sodium transporter proteins. Male Fisher 344 × Brown Norway (F344 × BN) rats of 3-, 10-, 24-, or 31 months of age (3M, 10M, 24M, or 31M) were either water restricted (WR) for 5 days or control (ad libitum water). Major renal sodium transporters and channel subunits were evaluated by immunoblotting and immunohistochemistry. Age did not significantly affect plasma arginine vasopressin or aldosterone levels, but renin activity was only 8% in 31M-WR rats relative to 3M-WR (P<0.05). Extreme aging (31M) led to decreased outer medullary abundance of the bumetanide-sensitive Na–K–2Cl cotransporter and decreased cortical abundance of the β- and γ-subunits (70-kDa band) of the epithelial sodium channel (ENaC) (P<0.05). Water restriction significantly (P<0.05) increased the abundance of Na–K–2Cl cotransporter (NKCC2) and Na–Cl cotransporter (NCC) across ages. However, these increases were significantly blunted as rats aged. Mean band densities were increased in WR rats (relative to age controls) by 54 and 106% at 3M, but only 25 and 29% at 24M and 0 and 6% at 31M for NKCC2 and NCC, respectively. Aged F344 × BN rats have reduced basal distal tubular renal sodium transporter abundances and blunted upregulation during water restriction, which may contribute to decreased urinary concentrating capacity

Human health risk assessment for aluminium, aluminium oxide, and aluminium hydroxide.

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