Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Deoxycorticosterone upregulates PDS (Slc26a4) in mouse kidney: role of pendrin in mineralocorticoid-induced hypertension.

Hypertension (Dallas, Tex. : 1979) - 1 Sept 2003

Verlander Jill W, Hassell Kathryn A, Royaux Ines E, Glapion Dawn M, Wang Mou-Er, Everett Lorraine A, Green Eric D, Wall Susan M

Abstract excerpt

Pendrin is an anion exchanger expressed along the apical plasma membrane and apical cytoplasmic vesicles of type B and of non-A, non-B intercalated cells of the distal convoluted tubule, connecting tubule, and cortical collecting duct. Thus, Pds (Slc26a4) is a candidate gene for the putative apical anion-exchange process of the type B intercalated cell. Because apical anion exchange-mediated transport is...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Blood Pressure
Share to Body Weight

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chlorides

Share to Microscopy, Immunoelectron

Share to Mineralocorticoids

Share to Potassium

Share to Sodium

Share to Sulfate Transporters

Source

Identifiers

PMID: 12925556
DOI: 10.1161/01.HYP.0000088321.67254.B7

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Deoxycorticosterone upregulates PDS (Slc26a4) in mouse kidney: role of pendrin in mineralocorticoid-induced hypertension.PMID 12925556Read ↗

Prostaglandin-E2 Mediated Increase in Calcium and Phosphate Excretion in a Mouse Model of Distal Nephron Salt Wasting.Semantic proximity Read ↗

Kidney collecting duct acid-base “regulon”Semantic proximity Read ↗

[Pendrin: its role in kidney function and hypertension].Semantic proximity Read ↗

[Pendrin: physiology, molecular biology and clinical importance].Semantic proximity Read ↗

SLC26A4 targeted to the endolymphatic sac rescues hearing and balance in Slc26a4 mutant mice.Semantic proximity Read ↗

Loss of cochlear HCO3- secretion causes deafness via endolymphatic acidification and inhibition of Ca2+ reabsorption in a Pendred syndrome mouse model.Semantic proximity Read ↗

Resistance to hypertension and high Cl- excretion in humans with SLC26A4 mutations.Semantic proximity Read ↗

Expression pattern of the mouse ortholog of the Pendred’s syndrome gene ( Pds ) suggests a key role for pendrin in the inner earSemantic proximity Read ↗

Genetics and phenomics of Pendred syndrome.Semantic proximity Read ↗

In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron.Semantic proximity Read ↗

Functional characterization of wild-type and mutated pendrin (SLC26A4), the anion transporter involved in Pendred syndrome.Semantic proximity Read ↗

Targeted mutation of SLC4A5 induces arterial hypertension and renal metabolic acidosis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.