Journal
AMERICAN JOURNAL OF NEPHROLOGY
Volume 28, Issue 5, Pages 860-870Publisher
KARGER
DOI: 10.1159/000139639
Keywords
diuretics; distal convoluted tubule; salt transport; potassium excretion; phosphorylation
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Funding
- NIDDK NIH HHS [R01 DK064635, DK-064635] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK064635] Funding Source: NIH RePORTER
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Two members of a recently discovered family of protein kinases are the cause of an inherited disease known as pseudohypoaldosteronism type II (PHAII). These patients exhibit arterial hypertension together with hyperkalemia and metabolic acidosis. This is a mirror image of Gitelman disease that is due to inactivating mutations of the SLC12A3 gene that encodes the thiazide-sensitive Na+ : Cl- cotransporter. The uncovered genes causing PHAII encode for serine/threonine kinases known as WNK1 and WNK4. Physiological and biochemical studies have revealed that WNK1 and WNK4 modulate the activity of several transport pathways of the aldosterone-sensitive distal nephron, thus increasing our understanding of how diverse renal ion transport proteins are coordinated to regulate normal blood pressure levels. Observations discussed in the present work place WNK1 and WNK4 as genes involved in the genesis of essential hypertension and as potential targets for the development of antihypertensive drugs. Copyright (C) 2008 S. Karger AG, Basel.
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