Calcium release from cardiac sarcoplasmic reticulum induced by photorelease of calcium or Ins(1,4,5)P3

Kentish, J. C.; Barsotti, Robert; Lea, T. J.; Mulligan, I. P.; Patel, Jitandrakumar R.; Ferenczi, Michael A.

doi:10.1152/ajpheart.1990.258.2.h610

Cited by 53 publications

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“…Inositol (1,4,5)trisphosphate is rapidly released into the cytoplasm, activates inositol(1,4,5) trisphosphate receptors in the sarcoplamic reticulum and causes Ca 2+ release from the sarcoplamic reticulum, which leads to vasoconstriction (Kleinz and Davenport, 2005). In normal cardiac cells, however, inositol(1,4,5)trisphosphate induced Ca 2+ release seems rather slow (Kentish et al, 1990). Nevertheless, it is known that Ca 2+ release from the sarcolpasmic reticulum is diminished as a result of hyperphosphorylation of the ryanodine receptors (Marks et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Apelin increases contractility in failing cardiac muscle

Dai

Ramírez-Correa

Gao

2006

European Journal of Pharmacology

132

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Apelin, a ligand for apelin-angiotension receptor-like 1 (APJ), has recently been shown to be a potent positive inotropic agent in normal hearts. In humans, levels of apelin have been shown to rise in early-stage heart failure and to fall in late-stage heart failure. In this study, we tested the hypothesis that apelin augments contraction directly in failing rat cardiac muscle. Right ventricular heart failure secondary to pulmonary hypertension was induced by exposing the rats to hypoxia (10% O 2 inhaled air) for 14-16 weeks. Trabeculae were dissected and mounted between a force transducer and a motor arm, superfused with Krebs-Henseleit (K-H) solution (pH 7.4, 22 °C), and loaded with fura-2.

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Section: Discussionmentioning

confidence: 99%

Apelin increases contractility in failing cardiac muscle

Dai

Ramírez-Correa

Gao

2006

European Journal of Pharmacology

132

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“…Functional studies on isolated animal ventricular fibers have shown that IP3 triggers calcium release from the SR (26) and potentiates the effects of caffeine-induced calcium release (27). Northern blot analyses using the cloned murine IP3R cDNA as a probe have identified the -10-kb IP3R mRNA in various mouse tissues, including the heart (7,28).…”

Section: Discussionmentioning

confidence: 99%

Differential regulation of two types of intracellular calcium release channels during end-stage heart failure.

Go¹,

Moschella²,

Watras³

et al. 1995

J. Clin. Invest.

224

136

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The molecular basis of human heart failure is unknown. Alterations in calcium homeostasis have been observed in failing human heart muscles. Intracellular calcium-release channels regulate the calcium flux required for muscle contraction. Two forms of intracellular calcium-release channels are expressed in the heart: the ryanodine receptor (RyR) and the inositol 1,4,5-trisphosphate receptor (LP3R).In the present study we showed that these two cardiac intracellular calcium release channels were regulated in opposite directions in failing human hearts. In the left ventricle, RyR mRNA levels were decreased by 31% (P < 0.025) whereas IP3R mRNA levels were increased by 123% (P < 0.005). In situ hybridization localized both RyR and IP3R mRNAs to human cardiac myocytes. The relative amounts of IP3 binding sites increased -40% compared with ryanodine binding sites in the failing heart. RyR down-regulation could contribute to impaired contractility; IP3R up regulation may be a compensatory'response providing an alternative'pathway for mobilizing intracellular calcium release, possibly contributing to the increased. diastolic tone associated with heart failure and the hypertrophic response of failing myocardium. (J. Clin. Invest. 1995. 95:888-894.)

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“…Indeed, the notion that IP 3 mediates Ca 2+ release in the heart is not new, and has been established by studies spanning the last two decades. The very earliest studies on cardiac IP 3 signaling found evidence for functional IP 3 Rs capable of releasing Ca 2+ from the SR [47][48][49][50][51]. However, compared with Ca 2+ -induced Ca 2+ release through RyRs, though, the IP 3 -induced Ca 2+ release was slow and small.…”

Section: The Dilemma Of Cardiac Ip 3 Receptors: Lost In An Ocean Of Rmentioning

confidence: 99%

Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes

Kockskämper

Zima

Roderick

et al. 2008

Journal of Molecular and Cellular Cardiology

172

149

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Inositol 1,4,5-trisphosphate (IP 3 ) is a ubiquitous intracellular messenger regulating diverse functions in almost all mammalian cell types. It is generated by membrane receptors that couple to phospholipase C (PLC), an enzyme which liberates IP 3 from phosphatidylinositol 4,5-bisphosphate (PIP 2 ). The major action of IP 3 , which is hydrophilic and thus translocates from the membrane into the cytoplasm, is to induce Ca 2+ release from endogenous stores through IP 3 receptors (IP 3 Rs). Cardiac excitation-contraction coupling relies largely on ryanodine receptor (RyR)-induced Ca 2+ release from the sarcoplasmic reticulum. Myocytes express a significantly larger number of RyRs compared to IP 3 Rs (∼100:1), and furthermore they experience substantial fluxes of Ca 2+ with each heartbeat. Therefore, the role of IP 3 and IP 3 -mediated Ca 2+ signaling in cardiac myocytes has long been enigmatic. Recent evidence, however, indicates that despite their paucity cardiac IP 3 Rs may play crucial roles in regulating diverse cardiac functions. Strategic localization of IP 3 Rs in cytoplasmic compartments and the nucleus enables them to participate in subsarcolemmal, bulk cytoplasmic and nuclear Ca 2+ signaling in embryonic stem cell-derived and neonatal cardiomyocytes, and in adult cardiac myocytes from the atria and ventricles. Intriguingly, expression of both IP 3 Rs and membrane receptors that couple to PLC/IP 3 signaling is altered in cardiac disease such as atrial fibrillation or heart failure, suggesting the involvement of IP 3 signaling in the pathology of these diseases. Thus, IP 3 exerts important physiological and pathological functions in the heart, ranging from the regulation of pacemaking, excitation-contraction and excitation-transcription coupling to the initiation and/or progression of arrhythmias, hypertrophy and heart failure. KeywordsInositol 1,4,5-trisphosphate; Cardiac myocyte; Calcium; Inotropy; Arrhythmias; Nucleus; Hypertrophy © 2008 Elsevier Inc. All rights reserved. * Corresponding author. E-mail address: jens.kockskaemper@meduni-graz.at (J. Kockskämper).. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript The discovery of IP 3A quarter of a century ago it was shown that D-myo inositol 1,4,5-trisphosphate (IP 3 ) releases Ca 2+ from a non-mitochondrial internal Ca 2+ store [1]. Since this hallmark discovery, IP 3 has emerged as a ubiquitous intracellular messenger, releasing Ca 2+ from stores through activation of IP 3 receptors (IP 3 Rs) in almost all eukaryotic cells. The major IP 3 -sensitive intracellular Ca 2+ store is the endoplasmic reticulum. However, IP 3 has also been shown to release Ca 2+ stored in other compartments, such as the Golgi and the nuclear envelope [2]. In addition, IP 3 Rs are present on the plasma membrane of some cell types, where they can gate Ca 2+ influx [3]. A crucial role for IP 3 -dependent Ca 2+ release has been demonstrated in many mammalian cell types, ranging from tiny platelets, where it initiates blood clottin...

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Calcium release from cardiac sarcoplasmic reticulum induced by photorelease of calcium or Ins(1,4,5)P3

Cited by 53 publications

References 0 publications

Apelin increases contractility in failing cardiac muscle

Apelin increases contractility in failing cardiac muscle

Differential regulation of two types of intracellular calcium release channels during end-stage heart failure.

Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes

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