Evidence map›Paper›PMID 11952152›Full record

ArticleMolecular and cellular biochemistry2002

Modulation of cardiac A1-adenosine receptors in rats following treatment with agents affecting heart rate.

Nissim Balas, Michael Arad, Babeth Rabinowitz, Asher Shainberg

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 55% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Purinergic signaling in thyroid disease.Purinergic signalling · 2023
    Review
  3. 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

4 authors at 1 institution in 1 country.

Nissim BalasThe Gonda-Goldschmied Medical Research Center, Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
Michael Arad
Babeth Rabinowitz
Asher Shainberg
Bar-Ilan University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Effects of chronic treatment affecting heart rate on A1 adenosine receptor levels and their functions were studied. Treatment of rats with isoproterenol for 10 days accelerated heart rate and increased the level of adenosine receptors, in both the atria and ventricles. Negative dromotropic response of isolated heart to adenosine was enhanced in isoproterenol-treated rats. Similar results were obtained following treatment with atropine sulfate, or swimming training but not after treatment with thyroxine. On the other hand, treatment with amiodarone, which normally causes a decrease in heart rate, also increased the level of adenosine receptors in both atria and ventricles. The sensitivity of the isolated heart to the negative dromotropic and chronotropic effects of adenosine was not enhanced in the amiodarone treated rats. Similar results were obtained following treatment with propranolol, while treatment with PTU (6-n-propyl-2-thiouracil) increased adenosine sensitivity in the isolated heart. It was concluded that the levels of A1 adenosine receptors in the heart correspond to heart rate, and to cardiac efficiency. While an increase in heart rate was followed by up-regulation of A1 adenosine receptors, a decrease in heart rate caused a moderate elevation of these receptors.

Indexed as

AdenosineAnimalsAtropineDown-RegulationHeart RateIsoproterenolMaleMyocardiumRatsRats, WistarReceptors, Purinergic P1SwimmingThyroxineUp-RegulationAdenosineAtropineIsoproterenolReceptors, Purinergic P1Thyroxine

Identifiers

PMID11952152
OpenAlexW257601587

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.