Evidence map›Paper›PMID 26082338›Full record

ArticleTherapeutic advances in cardiovascular disease2015

Modulation of cardiac L-type Ca2+ current by angiotensin-(1-7): normal versus heart failure.

Peng Zhou, Che Ping Cheng, Tiankai Li, Carlos M Ferrario, Heng-Jie Cheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Therapeutic advances in cardiovascular disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Cardiac remodelling and RAS inhibition.Therapeutic advances in cardiovascular disease · 2016
    Review
  9. Article
  10. 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 2 countries.

Peng ZhouSection on Cardiovascular Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Che Ping ChengSection on Cardiovascular Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Tiankai LiSection on Cardiovascular Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USADepartment of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Carlos M FerrarioDepartment of Surgery, Internal Medicine-Nephrology, and Physiology-Pharmacology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Heng-Jie ChengSection on Cardiovascular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157-1045, USAInstitute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA hcheng@wakehealth.edu.
Wake Forest University · US

Funding

New Molecular Target for Cardiac AgingR01AG049770 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHENG, HENG-JIE · 2015 to 2019
$1.6M
Beta3-Adrenergic Receptor &Progression to Heart FailureR01HL074318 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHENG, CHE-PING · 2003 to 2006
$1.3M
NHLBI NIH HHS HL074318NHLBI NIH HHS R01 HL074318NIA NIH HHS R01 AG049770
6 · The paper itself

Abstract

objectiveRecent evidence has shown that, in heart failure (HF), clinically relevant concentrations of angiotensin-(1-7) [Ang-(1-7)] counteracts angiotensin II induced cardiac depression and produces positive inotropic effects in both left ventricle (LV) and myocytes. However, the underlying electrophysiological mechanism is unclear. We investigated the role and mechanism of Ang-(1-7) on LV myocyte L-type calcium current (ICa,L) responses in normal state and in HF.

methodWe compared the effect of Ang-(1-7) (10(-5) M) on ICa,L responses in isolated LV myocytes obtained from 11 rats with isoproterenol (ISO) induced HF (3 months after 170 mg/kg subcutaneous for 2 days) and from 8 age-matched normal control rats by patch clamp technique.

resultsIn normal myocytes, compared with baseline, superfusion of Ang-(1-7) caused no significant changes in ICa,L (8.2 ± 0.2 versus 8.0 ± 0.3 pA/pF, p= not significant). In HF myocytes, the baseline ICa,L was significantly reduced (5.3 ± 0.1 versus 8.0 ± 0.3 pA/pF, p < 0.01). Ang-(1-7) produced a 21% increase in ICa,L (6.4±0.1 versus 5.3±0.1 pA/pF, p < 0.01). Pretreatment of HF myocytes with a nitric oxide (NO) synthase inhibitor (L-NAME, 10(-5) M) resulted in a significantly greater increase in ICa,L (28%, 8.4 ± 0.1 versus 6.5 ± 0.1 pA/pF, p < 0.01) during Ang-(1-7) superfusion. In contrast, during incubation with the bradykinin (BK) inhibitor HOE 140 (10(-6) M), Ang-(1-7) induced increase in ICa,L was significantly decreased. The Ang-(1-7) induced increase in ICa,L was abolished by [D-Ala(7)]-Ang-(1-7) (A-779, 10(-5) M).

conclusionsHF alters the response of ICa,L to Ang-(1-7). In normal myocytes, Ang-(1-7) has no significant effect on ICa,L. However, in HF myocytes, Ang-(1-7) increases ICa,L. These effects are mediated by the Ang-(1-7) Mas receptors and involve activation of NO/BK pathways.

Indexed as

Angiotensin IAnimalsBradykininCalcium Channels, L-TypeCalcium SignalingCardiotonic AgentsDisease Models, AnimalHeart FailureIsoproterenolMaleMembrane PotentialsMyocytes, CardiacNecrosisNitric OxidePeptide FragmentsProto-Oncogene MasAngiotensin Iangiotensin I (1-7)BradykininCalcium Channels, L-TypeCardiotonic AgentsIsoproterenolNitric OxidePeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupledcalciumheart failureion currentsreceptorsvasodilator agents

Identifiers

PMID26082338
PMCPMC4795833
OpenAlexW2334018857

What OpenQuestion holds

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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.