Evidence map›Paper›PMID 11711563›Full record

ArticleThe Journal of physiology2001

Inhibition of the formation or action of angiotensin II reverses attenuated K+ currents in type 1 and type 2 diabetes.

Y Shimoni

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 57 citations in OpenAlex.

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  9. Development and validation of a prognostic index for risk stratification of patients with early repolarization.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2012
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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 at 1 institution in 1 country.

Y ShimoniDepartment of Physiology and Biophysics, Cardiovascular Research Group, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1. shimoni@ucalgary.edu
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Transient and sustained calcium-independent outward K(+) currents (I(t) and I(SS)) as well as action potentials were recorded in cardiac ventricular myocytes isolated from two models of diabetes mellitus. 2. Rats injected (I.V.) with streptozotocin (STZ, 100 mg kg(-1)) 6-10 days before cell isolation developed insulin-dependent (type 1) diabetes. I(t) and I(SS) were attenuated and the action potential prolonged. Incubation of myocytes (6-9 h) with the angiotensin II (ATII) receptor blockers saralasin or valsartan (1 microM) significantly augmented these currents. Inclusion of valsartan (1 g l(-1)) in the drinking water for 5-10 days prior to and following STZ injection partially prevented current attenuation. 3. Incubation of myocytes from STZ-treated rats (6-9 h) with 1 microM quinapril, an angiotensin-converting enzyme (ACE) inhibitor, significantly augmented I(t) and I(SS) and shortened the ventricular action potential. I(t) augmentation was not due to changes in steady-state inactivation or in recovery from inactivation. No acute effects of quinapril were observed. 4. The effects of quinapril and valsartan were abolished by 2 microM cycloheximide. 5. Myocytes were isolated from the db/db mouse, a leptin receptor mutant that develops symptoms of non-insulin-dependent (type 2) diabetes. K+ currents in these cells were also attenuated, and the action potentials prolonged. Incubation of these cells (> 6 h) with valsartan (1 microM) significantly enhanced the transient and sustained outward currents. 6. These results confirm recent suggestions that cardiac myocytes contain a renin-angiotensin system, which is activated in diabetes. It is proposed that chronic release of ATII leads to changes in ionic currents and action potentials, which can be reversed by blocking the formation or action of ATII. This may underlie the proven benefits of ATII receptor blockade or ACE inhibition in diabetes, by providing protection against cardiac arrhythmias.

Indexed as

Receptors, Cell SurfaceTetrahydroisoquinolinesAction PotentialsAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin Receptor AntagonistsAnimalsCarrier ProteinsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Electric ConductivityIsoquinolinesMutationPotassium ChannelsQuinaprilAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin Receptor AntagonistsCarrier ProteinsIsoquinolinesPotassium ChannelsQuinaprilReceptor, Angiotensin, Type 2Receptors, Cell SurfaceReceptors, LeptinSaralasinTetrahydroisoquinolinesTetrazolesValineValsartan

Identifiers

PMID11711563
PMCPMC2278945
OpenAlexW2022669266

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.