Evidence map›Paper›PMID 10602335›Full record

ArticleBritish journal of pharmacology1999

Histamine H1-receptor-mediated modulation of the delayed rectifier K+ current in guinea-pig atrial cells: opposite effects on IKs and IKr.

Y Matsumoto, T Ogura, H Uemura, T Saito, Y Masuda, H Nakaya

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Stimulation of histamine HNaunyn-Schmiedeberg's archives of pharmacology · 2025
    Article
  3. Function and Role of Histamine HPharmaceuticals (Basel, Switzerland) · 2023
    Review
  4. The Roles of Cardiovascular HFrontiers in pharmacology · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

6 authors at 1 institution in 1 country.

Y MatsumotoThird Department of Internal Medicine, Chiba University School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Japan.
T Ogura
H Uemura
T Saito
Y Masuda
H Nakaya
Chiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Histamine receptor-mediated modulation of the rapid and slow components of the delayed rectifier K+ current (IK) was investigated in enzymatically-dissociated atrial cells of guinea-pigs using the whole cell configuration of the patch clamp technique. 2. Histamine at a concentration of 10 microM enhanced IK recorded during strong depolarization to potentials ranging from +20 to +40 mV and inhibited IK recorded during mild depolarization to potentials ranging from -20 to -10 mV. The increase of IK was more prominent with longer depolarizing pulses, whereas the inhibition of IK was more marked with shorter depolarizing pulses, suggesting that histamine enhances IKs (the slow component of IK) and inhibits IKr (the rapid component of IK). 3. The histamine-induced enhancement of IKs and inhibition of IKr were abolished by 3 microM chlorpheniramine but not by 10 microM cimetidine, suggesting that these opposite effects of histamine on IKr and IKs are mediated by H1-receptors. 4. In the presence of 5 microM E-4031, an IKr blocker, histamine hardly affected IK during mild depolarization although it enhanced IK during strong depolarization in a concentration-dependent manner. Histamine increased IKs with EC50 value of 0.7 microM. In the presence of 300 microM indapamide, an IKs blocker, histamine hardly affected IKs but inhibited IKr in a concentration-dependent manner. Histamine decreased IKr with IC50 value of 0.3 microM. 5. Pretreatment with 100 nM calphostin C or 30 nM staurosporine, protein kinase C inhibitors, abolished the histamine-induced enhancement of IKs, but failed to affect the histamine-induced inhibition of IKr. 6. We conclude that in guinea-pig atrial cells H1-receptor stimulation enhances IKs and inhibits IKr through different intracellular mechanisms.

Indexed as

Potassium Channels, Voltage-GatedAnimalsAtrial FunctionDelayed Rectifier Potassium ChannelsEnzyme ActivatorsGuinea PigsHeartHeart AtriaHistamineIntracellular FluidMembrane PotentialsPatch-Clamp TechniquesPotassium Channel BlockersPotassium ChannelsProtein Kinase CReceptors, Histamine H1Delayed Rectifier Potassium ChannelsEnzyme ActivatorsHistaminePotassium Channel BlockersPotassium ChannelsPotassium Channels, Voltage-GatedProtein Kinase CReceptors, Histamine H1

Identifiers

PMID10602335
PMCPMC1571771
OpenAlexW1971867334

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.