Evidence map›Paper›PMID 23585136›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2013

Inotropic and lusitropic effects of calcitonin gene-related peptide in the heart.

Mustafa Al-Rubaiee, Pandu R Gangula, Richard M Millis, Robin K Walker, Nsini A Umoh, Valerie M Cousins, Miara A Jeffress, Georges E Haddad

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Cardiorespiratory function associated with dietary nitrate supplementation.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2014
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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

8 authors at 3 institutions in 1 country.

Mustafa Al-RubaieeDepartment of Physiology and Biophysics, College of Medicine, Howard University, Washington, DC 20059, USA.
Pandu R Gangula
Richard M Millis
Robin K Walker
Nsini A Umoh
Valerie M Cousins
Miara A Jeffress
Georges E Haddad
University of Washington · USHoward University · USMeharry Medical College · US

Funding

STRUCTURAL/FUNCTIONAL CHARACTERIZATION OF AMINOGLYCOSIDEG12RR003048 · NCRR · HOWARD UNIVERSITY · PI SOUTHERLAND, WILLIAM M. · 1985 to 2011
$19.0M
MECHANISMS OF ALCOHOL-INDUCED CARDIOMYOPATHY.R15AA019816 · NIAAA · HOWARD UNIVERSITY · PI HADDAD, GEORGES E. · 2011 to 2011
$442k
NCRR NIH HHS 2G12 RR003048NIAAA NIH HHS 1 R15 AA-019816-01A1NIAAA NIH HHS R15 AA019816NIGMS NIH HHS GM-08016-38
6 · The paper itself

Abstract

Previous studies have demonstrated positive-inotropic effects of calcitonin gene-related peptide (CGRP), but the mechanisms remain unclear. Therefore, two experiments were performed to determine the physiological correlates of the positive-inotropic effects of CGRP. Treatments designed to antagonize the effects of physiologically active CGRP₁₋₃₇ included posttreatment with CGRP₈₋₃₇ and pretreatment with LY-294002 (LY, an inhibitor of phosphatidylinositol 3-kinase), 17β-estradiol (E), and progesterone (P) were also used to modulate the effects of CGRP₁₋₃₇. Experiment 1 was in vitro studies on sarcomeres and cells of isolated adult rat cardiac myocytes. CGRP₁₋₃₇, alone and in combination with E and P, decreased sarcomere shortening velocities and increased shortening percentages, effects that were antagonized by CGRP₈₋₃₇, but not by LY. CGRP₁₋₃₇ increased resting intracellular calcium ion concentrations and Ca(2+) influxes, effects that were also antagonized by both CGRP₈₋₃₇ and LY. Experiment 2 was in vivo studies on left ventricular pressure-volume (PV) loops. CGRP₁₋₃₇ increased end-systolic pressure, ejection fraction, and velocities of contraction and relaxation while decreasing stroke volume, cardiac output, stroke work, PV area, and compliance. After partial occlusion of the vena cava, CGRP₁₋₃₇ increased the slope of the end-systolic PV relationship. CGRP₈₋₃₇ and LY attenuated most of the CGRP-induced changes. These findings suggest that CGRP-induced positive-inotropic effects may be increased by treatments with estradiol and progesterone and inhibited by LY. The physiological correlates of CGRP-induced positive inotropy observed in rat sarcomeres, cells, and intact hearts are likely to reveal novel mechanisms of heart failure in humans.

Indexed as

Cardiotonic AgentsAnimalsCalcitonin Gene-Related PeptideCalciumCalcium SignalingCell SeparationEstradiolGonadal Steroid HormonesHeartMaleMyocardial ContractionMyocytes, CardiacPeptide FragmentsPhosphatidylinositol 3-KinasesProgesteroneRatsCalcitonin Gene-Related PeptideCalciumCardiotonic AgentsEstradiolGonadal Steroid HormonesPeptide FragmentsPhosphatidylinositol 3-KinasesProgesteronecalcitonin gene-related peptidecardiacestrogenPI3Kprogesterone

Identifiers

PMID23585136
PMCPMC3680720
OpenAlexW2066080840

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.