Evidence map›Paper›PMID 18216162›Full record

ArticleAmerican journal of physiology. Cell physiology2008

Apical maxi-K (KCa1.1) channels mediate K+ secretion by the mouse submandibular exocrine gland.

Tetsuji Nakamoto, Victor G Romanenko, Atsushi Takahashi, Ted Begenisich, James E Melvin

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 60 citations in OpenAlex.

  1. Potassium Channels of the Airway Epithelium.Acta physiologica (Oxford, England) · 2026
    Review
  2. Review
  3. Article
  4. CFTR expression in human salivary gland acinar cells.American journal of physiology. Cell physiology · 2024
    Article
  5. Article
  6. Article
  7. A Mathematical Model of Salivary Gland Duct Cells.Bulletin of mathematical biology · 2022
    Article
  8. Review
  9. Bio-protocol · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Knockout of the LRRC26 subunit reveals a primary role of LRRC26-containing BK channels in secretory epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Article
  18. Article
  19. Review
  20. Multiscale modelling of saliva secretion.Mathematical biosciences · 2014
    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

5 authors at 1 institution in 1 country.

Tetsuji NakamotoCenter for Oral Biology, Department of Pharmacology and Physiology, Univ. of Rochester Medical Center, Box 611, 601 Elmwood Ave, Rochester, NY 14642, USA.
Victor G Romanenko
Atsushi Takahashi
Ted Begenisich
James E Melvin
University of Rochester · US

Funding

PHYSIOLOGY OF MUCUS-SECRETING SALIVARY GLANDSR01DE008921 · NIDCR · UNIVERSITY OF ROCHESTER · PI OVITT, CATHERINE · 1989 to 2013
$2.9M
Physiology of Mucus-Secreting Salivary GlandsR37DE008921 · NIDCR · UNIVERSITY OF ROCHESTER · PI MELVIN, JAMES E · 2004 to 2009
$2.3M
The Physiological Roles of K Channels in Fluid SecretionR01DE016960 · NIDCR · UNIVERSITY OF ROCHESTER · PI BEGENISICH, TED B · 2006 to 2010
$1.8M
SPECIALIZED MATERIALS SCIENCE RESEARCH CENTERP50DE009296 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI O'BRIEN, WILLIAM J · 1989 to 1998
–
NIDCR NIH HHS DE-016960NIDCR NIH HHS DE-08921NIDCR NIH HHS DE-09296NIDCR NIH HHS R01 DE008921NIDCR NIH HHS R01 DE016960NIDCR NIH HHS R37 DE008921
6 · The paper itself

Abstract

The exocrine salivary glands of mammals secrete K+ by an unknown pathway that has been associated with HCO3(-) efflux. However, the present studies found that K+ secretion in the mouse submandibular gland did not require HCO3(-), demonstrating that neither K+/HCO3(-) cotransport nor K+/H+ exchange mechanisms were involved. Because HCO3(-) did not appear to participate in this process, we tested whether a K channel is required. Indeed, K+ secretion was inhibited >75% in mice with a null mutation in the maxi-K, Ca2+-activated K channel (KCa1.1) but was unchanged in mice lacking the intermediate-conductance IKCa1 channel (KCa3.1). Moreover, paxilline, a specific maxi-K channel blocker, dramatically reduced the K+ concentration in submandibular saliva. The K+ concentration of saliva is well known to be flow rate dependent, the K+ concentration increasing as the flow decreases. The flow rate dependence of K+ secretion was nearly eliminated in KCa1.1 null mice, suggesting an important role for KCa1.1 channels in this process as well. Importantly, a maxi-K-like current had not been previously detected in duct cells, the theoretical site of K+ secretion, but we found that KCa1.1 channels localized to the apical membranes of both striated and excretory duct cells, but not granular duct cells, using immunohistochemistry. Consistent with this latter observation, maxi-K currents were not detected in granular duct cells. Taken together, these results demonstrate that the secretion of K+ requires and is likely mediated by KCa1.1 potassium channels localized to the apical membranes of striated and excretory duct cells in the mouse submandibular exocrine gland.

Indexed as

AnimalsBicarbonatesCell MembraneCell PolarityIndolesIntermediate-Conductance Calcium-Activated Potassium ChannelsIon Channel GatingKineticsLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMembrane PotentialsMiceMice, KnockoutPotassiumPotassium Channel BlockersSalivaSodiumBicarbonatesIndolesIntermediate-Conductance Calcium-Activated Potassium ChannelsKcnma1 protein, mouseKcnn4 protein, mouseLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitspaxillinePotassiumPotassium Channel BlockersSodium

Identifiers

PMID18216162
PMCPMC3298180
OpenAlexW2137807092

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.