Acetylcholine Attenuates Hydrogen Peroxide-Induced Intracellular Calcium Dyshomeostasis Through Both Muscarinic and Nicotinic Receptors in Cardiomyocytes

Palee, Siripong; Apaijai, Nattayaporn; Shinlapawittayatorn, Krekwit; Chattipakorn, Siriporn C.; Chattipakorn, Nipon

doi:10.1159/000445628

Cited by 22 publications

(17 citation statements)

References 31 publications

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“…The heart tissues were frozen in liquid nitrogen immediately, and stored at −80 °C in preparation for western blot analysis. In addition, the other half of the rats from each group (n = 6/group) were deeply anesthetized with thiopental (0.5 mg/kg; Research institute of antibiotics and biotransformations, Roztoky, Czech Republic), and then the hearts of the rats were rapidly removed for single ventricular myocyte isolation71. Cardiomyocyte cells were isolated by using an enzymatic technique7172.…”

Section: Methodsmentioning

confidence: 99%

“…The Ca 2+ transient level in rat ventricular myocytes was measured using a fluorimetric ratio technique7172. The fluorescent Ca 2+ indicator Fura-2 was loaded by incubating the cardiomyocytes at room temperature for 30 minutes with 25 μM of Fura-2-AM (Sigma Chemical, St. Louis, MO, USA).…”

Section: Methodsmentioning

confidence: 99%

“…The ratio of the emission wavelengths is directly related to the amount of cardiac [Ca 2+ ]i74. The fluorescence ratio data was processed and stored in a computer using Xcellence imaging software (Olympus, Tokyo, Japan)7172.…”

Section: Methodsmentioning

confidence: 99%

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Restoring the impaired cardiac calcium homeostasis and cardiac function in iron overload rats by the combined deferiprone and N-acetyl cysteine

Wongjaikam

Kumfu

Khamseekaew

et al. 2017

Sci Rep

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Intracellular calcium [Ca2+]i dysregulation plays an important role in the pathophysiology of iron overload cardiomyopathy. Although either iron chelators or antioxidants provide cardioprotection, a comparison of the efficacy of deferoxamine (DFO), deferiprone (DFP), deferasirox (DFX), N-acetyl cysteine (NAC) or a combination of DFP plus NAC on cardiac [Ca2+]i homeostasis in chronic iron overload has never been investigated. Male Wistar rats were fed with either a normal diet or a high iron (HFe) diet for 4 months. At 2 months, HFe rats were divided into 6 groups and treated with either a vehicle, DFO (25 mg/kg/day), DFP (75 mg/kg/day), DFX (20 mg/kg/day), NAC (100 mg/kg/day), or combined DFP plus NAC. At 4 months, the number of cardiac T-type calcium channels was increased, whereas cardiac sarcoplasmic-endoplasmic reticulum Ca2+ ATPase (SERCA) was decreased, leading to cardiac iron overload and impaired cardiac [Ca2+]i homeostasis. All pharmacological interventions restored SERCA levels. Although DFO, DFP, DFX or NAC alone shared similar efficacy in improving cardiac [Ca2+]i homeostasis, only DFP + NAC restored cardiac [Ca2+]i homeostasis, leading to restoring left ventricular function in the HFe-fed rats. Thus, the combined DFP + NAC was more effective than any monotherapy in restoring cardiac [Ca2+]i homeostasis, leading to restored myocardial contractility in iron-overloaded rats.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Restoring the impaired cardiac calcium homeostasis and cardiac function in iron overload rats by the combined deferiprone and N-acetyl cysteine

Wongjaikam

Kumfu

Khamseekaew

et al. 2017

Sci Rep

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“…Interestingly, our data show that the effect of VNS on IR‐induced arginase upregulation was completely abolished in the presence of the α7 nAChR antagonist, indicating that the enhancement of myocardial arginase activation is particularly driven by inflammation. As the effect of VNS on infarct size was partially blocked by MLA, these results indicate that additional signalling pathways are implicated in the protective effect of VNS, for example VNS acting on mitochondrial function, stimulation of hypoxia inducible factor‐1 alpha‐related defence mechanism or reduced IR‐induced oxidative stress . In addition, the involvement of the activation of muscarinic receptors in VNS‐mediated cardioprotection should also be considered …”

Section: Discussionmentioning

confidence: 92%

“…As the effect of VNS on infarct size was partially blocked by MLA, these results indicate that additional signalling pathways are implicated in the protective effect of VNS, for example VNS acting on mitochondrial function, 29 stimulation of hypoxia inducible factor-1 alpha-related defence mechanism 30 or reduced IR-induced oxidative stress. 15,31 In addition, the involvement of the activation of muscarinic receptors in VNS-mediated cardioprotection should also be considered. 17 We next investigated the effect of VNS on arginase activity in the aorta.…”

Section: Figurementioning

confidence: 99%

Vagal nerve stimulation reduces infarct size via a mechanism involving the alpha‐7 nicotinic acetylcholine receptor and downregulation of cardiac and vascular arginase

et al. 2017

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Estrogen deprivation aggravates intracellular calcium dyshomeostasis in the heart of obese‐insulin resistant rats

Palee

Minta

Mantor

et al. 2018

Journal Cellular Physiology

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The incidence of cardiovascular disease and metabolic syndrome increases after the onset of menopause, giving evidence for the vital role of estrogen. Intracellular calcium [Ca 2+ ]i regulation plays an important role in the maintenance of left ventricular (LV) contractile function. Although either estrogen deprivation or obesity has been shown to strongly affect the metabolic status and LV function, the effects of estrogen deprivation on the cardiometabolic status and cardiac [Ca 2+ ]i regulation in the obese-insulin resistant condition have never been investigated. Our hypothesis was that estrogen deprivation aggravates LV dysfunction through the increased impairment of [Ca 2+ ]i homeostasis in obese-insulin resistant rats. Female rats were fed on either a high-fat (HFD, 59.28% fat) or normal (ND, 19.77% fat) diet for 13 weeks. Then, rats were divided into sham (HFS and NDS) operated or ovariectomized (HFO and NDO) groups. Six weeks after surgery, metabolic status, LV function and incidence of [Ca 2+ ]i transients were determined. NDO, HFS, and HFO rats had evidence of obese-insulin resistance indicated by increased body weight with hyperinsulinemia and euglycemia. Although NDO, HFS, and HFO rats had markedly reduced %LV fractional shortening, E/A ratio and decreased [Ca 2+ ]i transient amplitude and decay rate, HFO rats had the most severe impairments. These findings indicate that estrogen deprivation had a strong impact on abnormal LV function through [Ca 2+ ]i regulation. In addition, evidence was found that in obese-insulin resistant rats, estrogen deprivation severely aggravates LV dysfunction via increased impairment of [Ca 2+ ]i homeostasis.

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Acetylcholine Attenuates Hydrogen Peroxide-Induced Intracellular Calcium Dyshomeostasis Through Both Muscarinic and Nicotinic Receptors in Cardiomyocytes

Cited by 22 publications

References 31 publications

Restoring the impaired cardiac calcium homeostasis and cardiac function in iron overload rats by the combined deferiprone and N-acetyl cysteine

Restoring the impaired cardiac calcium homeostasis and cardiac function in iron overload rats by the combined deferiprone and N-acetyl cysteine

Vagal nerve stimulation reduces infarct size via a mechanism involving the alpha‐7 nicotinic acetylcholine receptor and downregulation of cardiac and vascular arginase

Estrogen deprivation aggravates intracellular calcium dyshomeostasis in the heart of obese‐insulin resistant rats

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