Evidence map›Paper›PMID 8680745›Full record

ArticleBritish journal of pharmacology1995

The involvement of ATP-sensitive potassium channels and adenosine in the regulation of coronary flow in the isolated perfused rat heart.

M D Randall

Abstract read
In one paragraph

Article in British journal of pharmacology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

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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

13 citing papers in PubMed.

  1. KPflugers Archiv : European journal of physiology · 2021
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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

1 author.

M D RandallDepartment of Physiology and Pharmacology, University of Nottingham Medical School, Queen's Medical Centre.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The roles of adenosine 5'-triphosphate (ATP)-sensitive potassium channels (KATP) and endogenous adenosine in the regulation of coronary flow have been assessed in the isolated, buffer-perfused heart of the rat. 2. In the presence of glibenclamide 10 microM there was a significant (P < 0.001) reduction in coronary flow from a baseline value of 8.78 +/- 0.76 ml min-1 g-1 to 3.89 +/- 0.59 ml min-1 g-1. This change was accompanied by a significant (P < 0.01) reduction in cardiac mechanical performance as shown by the decrease in the pressure-rate product from 21,487 +/- 2,577 mmHg min-1 to 6,950 +/- 1,104 mmHg min-1. 3. The non-selective adenosine antagonist 8-phenyltheophylline (10 microM) also caused a significant (P < 0.001) reduction in coronary flow from a basal value of 10.4 +/- 0.6 ml min-1 g-1 to 6.32 +/- 0.60 ml min-1 g-1. The subsequent addition of glibenclamide, in the presence of 8-phenyltheophylline, brought about a further significant (P < 0.001) reduction in coronary flow to 3.05 +/- 0.55 ml min-1 g-1 and this value was similar to that in the presence of glibenclamide alone. 4. In hearts perfused under constant flow conditions, exogenous adenosine caused dose-related reductions in coronary perfusion pressure described by a maximum reduction in pressure of 30.7 +/- 3.9 mmHg and an ED50 of 977 +/- 813 pmol. Addition of glibenclamide caused a significant (P < 0.01) increase in coronary perfusion pressure of 44.7 +/- 7.2 mmHg and a significant (P < 0.05) rightward shift of the dose-response curve for the depressor effects of adenosine (ED50 = 13.5 +/- 3.8 nmol), with a depression (P < 0.05) of the maximum (16.3 +/- 2.4 mmHg). 5. In conclusion, both KATP and endogenous adenosine make major contributions towards coronary vascular tone and the regulation of coronary flow in the rat isolated heart. Furthermore, in the coronary vasculature a significant proportion of the vasodilator action of adenosine is mediated through the activation of KATP.

Indexed as

AdenosineAdenosine TriphosphateAnimalsBenzopyransCoronary CirculationCromakalimGlyburideHeartIn Vitro TechniquesMalePerfusionPotassium ChannelsPyrrolesRatsRats, WistarTheophylline8-phenyltheophyllineAdenosineAdenosine TriphosphateBenzopyransCromakalimGlyburidePotassium ChannelsPyrrolesTheophyllineVasoconstrictor AgentsVasodilator Agents

Identifiers

PMID8680745
PMCPMC1909199

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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.