The physiology of cardiac calcium handling

Bögeholz, Nils; Muszyński, A; Pott, Christian

doi:10.1007/s10354-012-0102-3

Cited by 7 publications

(8 citation statements)

References 12 publications

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“…However, the major stimulus for controlling PLB activity is related to the β adrenergic system, since it PLB phosphorylation at serine 16 regulates SERCA2a activity, which may hampering or not recapturing Ca 2+ from sarcoplasmic reticulum. This injury is related to lusitropic damage to cardiac tissue [ 68 ]. The transcription signal or signals responsible for triggering the actions of the β-adrenergic system grafting occur because catecholamines or adrenergic agonists bind to their receptors, acting as first messenger in the β-adrenergic pathway.…”

Section: Discussionmentioning

confidence: 99%

“…This cascade of events leads to changes in the activity of proteins including L-type calcium channels [ 26 , 69 ], phospholamban [ 70 ], troponin I [ 71 ] and ryanodine receptors [ 72 ], altering cardiac function [ 22 ]. Thus, the adrenergic stimulation increases the inotropy (contractile force), chronotropy (heart rate), dromotropy (excitation conductance), bathmotropy (decrease in threshold of excitation) and lusitropy (relaxation) of cardiac tissue [ 68 ].…”

Section: Discussionmentioning

confidence: 99%

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Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway

et al. 2015

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Obesity has been shown to impair myocardial performance. Some factors have been suggested as responsible for possible cardiac abnormalities in models of obesity, among them beta-adrenergic (βA) system, an important mechanism of regulation of myocardial contraction and relaxation. The objective of present study was to evaluate the involvement of βA system components in myocardial dysfunction induced by obesity. Thirty-day-old male Wistar rats were distributed in control (C, n = 25) and obese (Ob, n = 25) groups. The C group was fed a standard diet and Ob group was fed four unsaturated high-fat diets for 15 weeks. Cardiac function was evaluated by isolated papillary muscle preparation and βA system evaluated by using cumulative concentrations of isoproterenol and Western blot. After 15 weeks, the Ob rats developed higher adiposity index than C rats and several comorbidities; however, were not associated with changes in systolic blood pressure. Obesity caused structural changes and the myocardial responsiveness to post-rest contraction stimulus and increased extracellular calcium (Ca2+) was compromised. There were no changes in cardiac function between groups after βA stimulation. The obesity was not accompanied by changes in protein expression of G protein subunit alpha (Gsα) and βA receptors (β1AR and β2AR). In conclusion, the myocardial dysfunction caused by unsaturated high-fat diet-induced obesity, after 15 weeks, is not related to βAR system impairment at the receptor-signalling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway

et al. 2015

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“…However, there are only a few studies that have reported impaired intracellular Ca 2+ handling leading to myocardial dysfunction in OR rodents. In cardiac myocytes, Ca 2+ plays an important role in cardiac performance and physiological processes 15 , 36 . According to Bögeholz et al 36 , there are three main ways to modulate the contractile function of myofilaments, namely (1) alteration of cytosolic Ca 2+ concentration, (2) mechanical change in pretension, and (3) catecholaminergic stimulation.…”

Section: Discussionmentioning

confidence: 99%

Obesity Resistance Promotes Mild Contractile Dysfunction Associated with Intracellular Ca²⁺Handling

Sá

Leopoldo

Jacobsen

et al. 2015

Arquivos Brasileiros De Cardiologia

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BackgroundDiet-induced obesity is frequently used to demonstrate cardiac dysfunction. However, some rats, like humans, are susceptible to developing an obesity phenotype, whereas others are resistant to that.ObjectiveTo evaluate the association between obesity resistance and cardiac function, and the impact of obesity resistance on calcium handling.MethodsThirty-day-old male Wistar rats were distributed into two groups, each with 54 animals: control (C; standard diet) and obese (four palatable high-fat diets) for 15 weeks. After the experimental protocol, rats consuming the high-fat diets were classified according to the adiposity index and subdivided into obesity-prone (OP) and obesity-resistant (OR). Nutritional profile, comorbidities, and cardiac remodeling were evaluated. Cardiac function was assessed by papillary muscle evaluation at baseline and after inotropic maneuvers.ResultsThe high-fat diets promoted increase in body fat and adiposity index in OP rats compared with C and OR rats. Glucose, lipid, and blood pressure profiles remained unchanged in OR rats. In addition, the total heart weight and the weight of the left and right ventricles in OR rats were lower than those in OP rats, but similar to those in C rats. Baseline cardiac muscle data were similar in all rats, but myocardial responsiveness to a post-rest contraction stimulus was compromised in OP and OR rats compared with C rats.ConclusionObesity resistance promoted specific changes in the contraction phase without changes in the relaxation phase. This mild abnormality may be related to intracellular Ca2+ handling.

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“…The probability of acto-myosin binding is therefore associated with increased intracellular calcium concentration. 29 Changes in the calcium transient directly affect contraction and relaxation dynamics and short- and long-term power output of the heart, making it a potent regulator of transient and long-term cardiac mechanotransduction. 30 …”

Section: The Sarcomerementioning

confidence: 99%

From Stem Cells to Cardiomyocytes

Kaushik¹,

Engler²

2014

Progress in Molecular Biology and Translational Science

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Stem cell differentiation into a variety of lineages is known to involve signaling from the extracellular niche, including from the physical properties of that environment. What regulates stem cell responses to these cues is there ability to activate different mechanotransductive pathways. Here, we will review the structures and pathways that regulate stem cell commitment to a cardiomyocyte lineage, specifically examining proteins within muscle sarcomeres, costameres, and intercalated discs. Proteins within these structures stretch, inducing a change in their phosphorylated state or in their localization to initiate different signals. We will also put these changes in the context of stem cell differentiation into cardiomyocytes, their subsequent formation of the chambered heart, and explore negative signaling that occurs during disease.

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The physiology of cardiac calcium handling

Cited by 7 publications

References 12 publications

Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway

Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway

Obesity Resistance Promotes Mild Contractile Dysfunction Associated with Intracellular Ca²⁺Handling

From Stem Cells to Cardiomyocytes

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The physiology of cardiac calcium handling

Cited by 7 publications

References 12 publications

Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway

Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway

Obesity Resistance Promotes Mild Contractile Dysfunction Associated with Intracellular Ca2+Handling

From Stem Cells to Cardiomyocytes

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Obesity Resistance Promotes Mild Contractile Dysfunction Associated with Intracellular Ca²⁺Handling