Evidence map›Paper›PMID 21816753›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Role of NKCC in BK channel-mediated net K⁺ secretion in the CCD.

Wen Liu, Carlos Schreck, Richard A Coleman, James B Wade, Yubelka Hernandez, Beth Zavilowitz, Richard Warth, Thomas R Kleyman, Lisa M Satlin

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. GDF15, an Emerging Player in Renal Physiology and Pathophysiology.International journal of molecular sciences · 2024
    Review
  3. Renal KFrontiers in physiology · 2023
    Review
  4. Potassium homeostasis: sensors, mediators, and targets.Pflugers Archiv : European journal of physiology · 2022
    Review
  5. L-WNK1 is required for BK channel activation in intercalated cells.American journal of physiology. Renal physiology · 2021
    Article
  6. Review
  7. Furosemide reduces BK-αβ4-mediated KAmerican journal of physiology. Renal physiology · 2019
    Article
  8. The renal response to potassium stress: integrating past with present.Current opinion in nephrology and hypertension · 2017
    Review
  9. The ZnBiochimica et biophysica acta. Molecular basis of disease · 2017
    Article
  10. Article
  11. Article
  12. Maintaining KAmerican journal of physiology. Renal physiology · 2016
    Review
  13. Review
  14. Cell-specific regulation of L-WNK1 by dietary K.American journal of physiology. Renal physiology · 2016
    Article
  15. Article
  16. Dietary potassium and the renal control of salt balance and blood pressure.Pflugers Archiv : European journal of physiology · 2015
    Review
  17. Generation of WNK1 knockout cell lines by CRISPR/Cas-mediated genome editing.American journal of physiology. Renal physiology · 2015
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Wen LiuDivision of Pediatric Nephrology, Department of Pediatrics, Mount Sinai School of Medicine, New York, New York 10029, USA.
Carlos Schreck
Richard A Coleman
James B Wade
Yubelka Hernandez
Beth Zavilowitz
Richard Warth
Thomas R Kleyman
Lisa M Satlin
Icahn School of Medicine at Mount Sinai · USUniversity of Maryland, Baltimore · USUniversity of Pittsburgh · USUniversity of Regensburg · DE

Funding

Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2008 to 2022
$13.4M
Regulation of K and H secretion by intercalated cellsR01DK038470 · NIDDK · YESHIVA UNIVERSITY · PI HUGHEY, REBECCA P, KLEYMAN, THOMAS R · 1994 to 2022
$7.7M
Biomechanical Regulation of Renal Ion TransportersR37DK051391 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2006 to 2015
$3.2M
STRUCTURE/FUNCTION ANALYSIS OF VASOPRESSIN ACTIONR01DK032839 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI WADE, JAMES B · 1986 to 2013
$3.0M
SODIUM CHANNELS IN THE MAMMALIAN URINARY BLADDERR01DK051391 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R. · 1996 to 2005
$1.5M
RENAL INTERCALATED CELL REGULATION AND DIFFERENTIATIONR29DK038470 · NIDDK · YESHIVA UNIVERSITY · PI SATLIN, LISA M. · 1986 to 1990
–
NIDDK NIH HHS DK038470NIDDK NIH HHS DK051391NIDDK NIH HHS DK32839NIDDK NIH HHS P30 DK079307NIDDK NIH HHS R01 DK038470NIDDK NIH HHS R37 DK051391
6 · The paper itself

Abstract

Apical SK/ROMK and BK channels mediate baseline and flow-induced K secretion (FIKS), respectively, in the cortical collecting duct (CCD). BK channels are detected in acid-base transporting intercalated (IC) and Na-absorbing principal (PC) cells. Although the density of BK channels is greater in IC than PC, Na-K-ATPase activity in IC is considered inadequate to sustain high rates of urinary K secretion. To test the hypothesis that basolateral NKCC in the CCD contributes to BK channel-mediated FIKS, we measured net K secretion (J(K)) and Na absorption (J(Na)) at slow (∼1) and fast (∼5 nl·min(-1)·mm(-1)) flow rates in rabbit CCDs microperfused in vitro in the absence and presence of bumetanide, an inhibitor of NKCC, added to the bath. Bumetanide inhibited FIKS but not basal J(K), J(Na), or the flow-induced [Ca(2+)](i) transient necessary for BK channel activation. Addition of luminal iberiotoxin, a BK channel inhibitor, to bumetanide-treated CCDs did not further reduce J(K). Basolateral Cl removal reversibly inhibited FIKS but not basal J(K) or J(Na). Quantitative PCR performed on single CCD samples using NKCC1- and 18S-specific primers and probes and the TaqMan assay confirmed the presence of the transcript in this nephron segment. To identify the specific cell type to which basolateral NKCC is localized, we exploited the ability of NKCC to accept NH(4)(+) at its K-binding site to monitor the rate of bumetanide-sensitive cytosolic acidification after NH(4)(+) addition to the bath in CCDs loaded with the pH indicator dye BCECF. Both IC and PC were found to have a basolateral bumetanide-sensitive NH(4)(+) entry step and NKCC1-specific antibodies labeled the basolateral surfaces of both cell types in CCDs. These results suggest that BK channel-mediated FIKS is dependent on a basolateral bumetanide-sensitive, Cl-dependent transport pathway, proposed to be NKCC1, in both IC and PC in the CCD.

Indexed as

AnimalsBumetanideCalciumCationsDiureticsFluorescent DyesImmunohistochemistryKidney CortexKidney Tubules, CollectingLarge-Conductance Calcium-Activated Potassium ChannelsMaleNephronsPeptidesPotassiumPotassium Channel BlockersQuaternary Ammonium CompoundsBumetanideCalciumCationsDiureticsFluorescent DyesiberiotoxinLarge-Conductance Calcium-Activated Potassium ChannelsPeptidesPotassiumPotassium Channel BlockersQuaternary Ammonium CompoundsRNA, MessengerSlc12a2 protein, ratSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2

Identifiers

PMID21816753
PMCPMC3280697
OpenAlexW2114408390

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.