Overexpression of Pendrin in Intercalated Cells Produces Chloride-Sensitive Hypertension

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Overexpression of pendrin in intercalated cells produces chloride-sensitive hypertension.

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 ...

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Dietary Cl(-) restriction upregulates pendrin expression within the apical plasma membrane of type B intercalated cells.

Pendrin, encoded by Slc26a4, is a Cl(-)/HCO(3)(-) exchanger expressed in the apical region of type B and non-A, non-B intercalated cells, which regulates renal NaCl excretion. Dietary Cl(-) restriction upregulates total pendrin protein expression. Whether the subcellular expression of pendrin and whether the apparent vascular volume contraction observed in Slc26a4 null mice are Cl(-) dependent,...

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Role of chloride in angiotensin II-induced salt-sensitive hypertension.

The present study investigated the effect of the anion accompanying sodium on the development of angiotensin II-induced hypertension in rats and the role of the sympathetic nervous system and extracellular fluid volume in its mechanism. Hypertension was induced by intraperitoneal infusion of angiotensin II (125 ng/min) for 12 days via miniosmotic pump. High dietary intake of sodium chloride sig...

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The emerging role of pendrin in renal chloride reabsorption.

RENAL REABSORPTION OF SODIUM and chloride is tightly linked in most segments, often occurring even through the same transport proteins such as the Na-K-2Cl cotransporter NKCC2 or the Na-Cl cotransporter NCC in the thick ascending limb or the distal tubule, respectively (1, 6). In the proximal tubule and in parts of the collecting system, the transport of chloride and sodium is mediated by separ...

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Sympathetic stimulation of thiazide-sensitive sodium chloride cotransport in the generation of salt-sensitive hypertension.

Excessive renal efferent sympathetic nerve activity contributes to hypertension in many circumstances. Although both hemodynamic and tubular effects likely participate, most evidence supports a major role for α-adrenergic receptors in mediating the direct epithelial stimulation of sodium retention. Recently, it was reported, however, that norepinephrine activates the thiazide-sensitive NaCl cot...

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ژورنال

عنوان ژورنال: Journal of the American Society of Nephrology

سال: 2013

ISSN: 1046-6673,1533-3450

DOI: 10.1681/asn.2012080787