Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2003 Apr;111(7):947-50.
doi: 10.1172/JCI18232.

Negative regulators of sodium transport in the kidney: key factors in understanding salt-sensitive hypertension?

Bernard C Rossier  1
Affiliations
Review

Negative regulators of sodium transport in the kidney: key factors in understanding salt-sensitive hypertension?

Bernard C Rossier. J Clin Invest. 2003 Apr.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
Diagram of the urinary sytem. The components comprising the aldosterone-sensitive distal nephron are shown in bright yellow.
Figure 2
Figure 2
Location of Na-Cl transporters and their regulatory proteins along the aldosterone-sensitive distal nephron. Sodium balance is ultimately achieved in this part of the renal tubule by fine aldosterone-mediated regulation of apically located Na-Cl cotransporters in the distal convoluted tubule (DCT); the epithelial sodium channel (ENaC) in the collecting duct (CD), connecting tubule (CNT), and overlapping expression in the distal convoluted tubule 2 (DCT2); and the aquaporin water transporter 2 (AQP2), which are all limiting factors in transepithelial fluid reabsorption (see review in ref. 11). The aldosterone-sensitive distal nephron expresses genes needed for the specificity of the aldosterone signaling cascade, i.e. the mineralocorticoid receptor (MR) and 11-βHSD2, an enzyme that protects MR from illicit occupation by cortisol. Mutations in these genes also cause severe salt-sensitive hypertensive phenotypes (see recent reviews in refs. and 12). TAL, thin ascending limb; CCD, cortical collecting duct; NKCC2, Na-K-2Cl cotransporter; SGK1, serum glucocorticoid–regulated kinase. Figure adapted with permission from Kriz and Kaissling (13), and Loffing and Kaissling (11).
See this image and copyright information in PMC

Comment on

References

    1. Guyton AC. Blood pressure control - Special role of the kidneys and body fluid. Science. 1991;252:1813–1816. - PubMed
    1. Lifton RP, Gharavi AG, Geller DS. Molecular mechanisms of human hypertension. Cell. 2001;104:545–556. - PubMed
    1. Achard JM, Disse-Nicodeme S, Fiquet-Kempf B, Jeunemaitre X. Phenotypic and genetic heterogeneity of familial hyperkalaemic hypertension (Gordon syndrome) Clin. Exp. Pharmacol. Physiol. 2001;28:1048–1052. - PubMed
    1. Wilson FH, et al. Human hypertension caused by mutations in WNK kinases. Science. 2001;293:1107–1112. - PubMed
    1. Choate KA, et al. WNK1, a kinase mutated in inherited hypertension with hyperkalemia, localizes to diverse Cl-transporting epithelia. Proc. Natl. Acad. Sci. U. S. A. 2003;100:663–668. - PMC - PubMed