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• W2068347291 abstract "Inherited and acquired disorders that enhance the activity of transporters mediating renal tubular Na+ reabsorption are well established causes of hypertension. It is unclear, however, whether primary activation of an Na+-independent chloride transporter in the kidney can also play a pathogenic role in this disease. Here, mice overexpressing the chloride transporter pendrin in intercalated cells of the distal nephron (TgB1-hPDS mice) displayed increased renal absorption of chloride. Compared with normal mice, these transgenic mice exhibited a delayed increase in urinary NaCl and ultimately, developed hypertension when exposed to a high-salt diet. Administering the same sodium intake as NaHCO3 instead of NaCl did not significantly alter BP, indicating that the hypertension in the transgenic mice was chloride-sensitive. Moreover, excessive chloride absorption by pendrin drove parallel absorption of sodium through the epithelial sodium channel ENaC and the sodium-driven chloride/bicarbonate exchanger (Ndcbe), despite an appropriate downregulation of these sodium transporters in response to the expanded vascular volume and hypertension. In summary, chloride transport in the distal nephron can play a primary role in driving NaCl transport in this part of the kidney, and a primary abnormality in renal chloride transport can provoke arterial hypertension. Thus, we conclude that the chloride/bicarbonate exchanger pendrin plays a major role in controlling net NaCl absorption, thereby influencing BP under conditions of high salt intake." @default.
• W2068347291 created "2016-06-24" @default.
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• W2068347291 date "2013-07-01" @default.
• W2068347291 modified "2023-10-17" @default.
• W2068347291 title "Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension" @default.
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• W2068347291 doi "https://doi.org/10.1681/asn.2012080787" @default.
• W2068347291 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3699825" @default.
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