Evidence map›Paper›PMID 23510939›Full record

ArticleChannels (Austin, Tex.)

β-adrenergic stimulation increases the intra-SR Ca termination threshold for spontaneous Ca waves in cardiac myocytes.

Joshua T Maxwell, Timothy L Domeier, Lothar A Blatter

Abstract readComment
In one paragraph

Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Joshua T MaxwellDepartment of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, IL, USA.
Timothy L Domeier
Lothar A Blatter

Funding

Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
E/C COUPLING AND CALCIUM REGULATION IN ATRIAL MYOCYTESR01HL062231 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI BLATTER, LOTHAR A · 1999 to 2012
$4.4M
MItochondrial Dysfunction in Cardiac Hypertrophy and FailureR01HL101235 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BERS, DONALD M, BLATTER, LOTHAR A · 2010 to 2013
$2.8M
Cardiomyocyte stretch and intracellular calcium release with advancing ageK01AG041208 · NIA · UNIVERSITY OF MISSOURI-COLUMBIA · PI DOMEIER, TIMOTHY LEE · 2012 to 2016
$545k
IP3R-Dependent Signaling in Excitation-Contraction Coupling during Heart FailureF32HL090211 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI DOMEIER, TIMOTHY LEE · 2007 to 2008
$97k
NHLBI NIH HHS F32 HL090211NHLBI NIH HHS F32HL090211NHLBI NIH HHS HL101235NHLBI NIH HHS HL62231NHLBI NIH HHS HL80101NHLBI NIH HHS P01 HL080101NHLBI NIH HHS R01 HL062231NHLBI NIH HHS R01 HL101235NIA NIH HHS 1K01AG041208NIA NIH HHS K01 AG041208
6 · The paper itself

Abstract

β-adrenergic stimulation of cardiac myocytes enhances intracellular calcium cycling, which frequently associates with pro-arrhythmic Ca waves. The threshold level of free calcium in the sarcoplasmic reticulum ([Ca]SR) where waves initiate is increased during β-adrenergic stimulation. ( 1) Here, we measured [Ca]SR directly to monitor the [Ca]SR level at which spontaneous Ca waves terminated (termination threshold) during β-adrenergic stimulation. Compared with control conditions, application of the β-adrenergic receptor agonist isoproterenol (ISO; 1 μM) resulted in an increase in basal [Ca]SR and an increase in the [Ca]SR at which spontaneous Ca waves terminated. When [Ca]SR was experimentally matched, ISO stimulation resulted in a decrease in the depletion amplitude of the waves. Sensitization of ryanodine receptor SR Ca release channels to Ca with a low dose of caffeine in the presence of ISO was able to decrease the termination threshold compared with control conditions. Therefore, the Ca wave termination level may represent an important mode of altering Ca depletion from the SR and reducing the arrhythmogenic potential during β-adrenergic stimulation.

Indexed as

AnimalsCalciumMaleMyocytes, CardiacReceptors, Adrenergic, betaSarcoplasmic ReticulumCalciumReceptors, Adrenergic, betaarrhythmiabeta-adrenergic stimulationCa wavesexcitation-contraction couplingintra-SR [Ca]ryanodine receptorventricular myocytes

Identifiers

PMID23510939
PMCPMC3710347

What OpenQuestion holds

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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.