Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes.

Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes. Abstract Text:

Aleksey V Zima,Jens ,Lothar A Blatter,

Localization of glycolytic enzymes in close proximity to Ca(2+) transport systems of the sarcoplasmic reticulum (SR) in cardiac cells suggests an important functional role for glycolysis in intracellular [Ca(2+)] regulation and, consequently, excitation-contraction coupling. Here, we investigated the mechanisms of regulation of SR Ca(2+) release by glycolytic sugar phosphate intermediates in cat ventricular myocytes. Experiments with permeabilized myocytes revealed that with normal cytosolic energy reserves (mm: ATP 5, ADP 0.01, phosphocreatine (CrP) 10) fructose-1,6-bisphosphate (FBP; 1 mm) and fructose-6-phosphate (F6P; 1 mm) caused a transient increase of Ca(2+) spark frequency by 62 and 42%, respectively. This effect of sugar phosphates was associated with a 13% decrease in SR Ca(2+) load. Pretreatment of the cells with an inhibitor of glycolysis, iodoacetate (IAA; 0.5 mm), did not prevent the effects of FBP and F6P on Ca(2+) sparks. Recording of single ryanodine receptor (RyR) channel activity indicated that FBP and F6P significantly increased RyR open probability. Reduction of cytosolic energy reserves decreased Ca(2+) spark activity. Increasing [ADP] to 0.4 mm or removal of CrP ([ATP] was kept constant) caused a slowly developing decrease of Ca(2+) spark frequency by 29 and 42%, respectively. Changing [ADP] and [CrP] simultaneously decreased Ca(2+) spark frequency by 66%. This inhibition of Ca(2+) sparks was associated with a 40% decrease in SR Ca(2+) load. The subsequent addition of FBP (1 mm) partially restored Ca(2+) spark frequency and SR Ca(2+) load. This recovery of Ca(2+) sparks was blocked completely by IAA. These data suggest that at physiological ATP, ADP and CrP levels accumulation of sugar phosphates from glycolysis can stimulate SR Ca(2+) release. This effect does not require the activity of downstream glycolytic enzymes, but rather is the result of direct activation of RyRs. However, under conditions associated with depletion of cellular energy reserves (e.g. myocardial ischaemia), ATP generated from glycolysis may play an important role in maintaining myocardial Ca(2+) homeostasis by improving SR Ca(2+) uptake.

Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes. Publishing Authors By Initials

AV Zima,J ,LA Blatter,

For similar carbohydrates: sugar phosphates research abstracts see: carbohydrates: sugar phosphates research

PUBMED ID PMID:

MEDLINE DATE:

Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of physiology

VOLUME: 577

Page Numbers: 281-93

Journal Abbreviation: J. Physiol. (Lond.)

ISSN: 0022-3751

DAY: 31

MONTH: 08

YEAR: 2006

Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 266262

Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes. Keywords Mesh Terms:

KEYWORDS: Sugar Phosphates

MESH TERMS: administration & dosage

Chemical & Substance for Abstract: Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes. Information

Substance Name: Calcium

Registry Number: 7440-70-2

Grant and Affiliation Information for Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes.

AFFILIATION: Department of Physiology, Stritch School of Medicine, Loyola University Chicago, 2160 South First Avenue, Maywood, IL 60153, USA.

Country: England

AGENCY: United States NHLBI

GRANT: R01HL62231

ACRONYM: HL

MEDLINETA: J Physiol

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes Related Publications

• Amplitude mode in the quantum phase model.
• Anisotropy of nickel release and corrosion in austenitic stainless steels.
• Ca2+ entry-independent effects of L-type Ca2+ channel modulators on Ca2+ sparks in ventricular myocytes.
• Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes.
• Effects of exchange symmetry on full counting statistics.
• Frontal lobe lesions, diffuse damage, and neuropsychological functioning in traumatic brain-injured patients.
• IP3 receptor-dependent Ca2+ release modulates excitation-contraction coupling in rabbit ventricular myocytes.
• IP3-dependent nuclear Ca2+ signalling in the mammalian heart.
• Integration of rapid cytosolic Ca2+ signals by mitochondria in cat ventricular myocytes.
• Joint free-energy distribution in the random directed polymer problem.
• MR imaging and MR angiography in the evaluation of pulsatile tinnitus.
• Mitochondrial Ca(2+) and the heart.
• N-particle scattering matrix for electrons interacting on a quantum dot.
• Partial inhibition of sarcoplasmic reticulum ca release evokes long-lasting ca release events in ventricular myocytes: role of luminal ca in termination of ca release.
• Redox regulation of cardiac calcium channels and transporters.
• Termination of cardiac Ca2+ sparks: role of intra-SR [Ca2+], release flux, and intra-SR Ca2+ diffusion.
• The effect of oxidative stress on Ca(2+) release and capacitative Ca(2+) entry in vascular endothelial cells.
• [Radius-head fractures]