Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 285, Issue 40, Pages 30363-30369Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.R110.155341
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Funding
- National Institutes of Health [DK078679, DK056695, DK085101, DK065161, DK054354]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K01DK078679, R01DK056695, R01DK054354, R56DK065161, R01DK085101, R01DK065161] Funding Source: NIH RePORTER
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The kidney has a central role in the regulation of blood pressure, in large part through its role in the regulated reabsorption of filtered Na+. Epithelial Na+ channels (ENaCs) are expressed in the most distal segments of the nephron and are a target of volume regulatory hormones. A variety of factors regulate ENaC activity, including several aldosterone-induced proteins that are present within an ENaC regulatory complex. Proteases also regulate ENaC by cleaving the channel and releasing intrinsic inhibitory tracts. Polymorphisms or mutations within channel subunits or regulatory pathways that enhance channel activity may contribute to an increase in blood pressure in individuals with essential hypertension.
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