Food restriction impairs myocardial inotropic response to calcium and β-adrenergic stimulation in spontaneously hypertensive rats

Gut, Ana Lúcia; Sugizaki, Mário Mateus; Okoshi, Marina Politi; Carvalho, Robson Francisco; Dal-Pai-Silva, Maeli; Aragon, Flávio Ferrari; Padovani, Carlos Roberto; Okoshi, Katashi; Cicogna, Antônio Carlos

doi:10.1016/j.nutres.2008.06.001

Cited by 7 publications

(10 citation statements)

References 34 publications

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“…Nevertheless, the lower response of food restricted rats to the increase of extracellular Ca 2+ concentration can be related to changes in the general mechanisms involved in Ca 2+ cycling such as sarcolemmal Na + /Ca 2+ exchanger, sarcolemmal L-type channel, sarcoplasmic reticulum (SR), ryanodine receptor, SR Ca 2+ uptake pump, and the myofilament Ca 2+ sensitivity. 35 In relation to RF, this process may be faster and more balanced, but no study was found to support this statement and show the activity and protein expression of Ca 2+ handling regulatory proteins.…”

Section: Discussionmentioning

confidence: 98%

“…Few studies have evaluated the β-adrenergic components in experimental models of fasting/refeeding. 25 , 35 Some studies have shown that cardiac function impairment is related to β-adrenergic system changes, 35 while other researchers have not reported reduced β-adrenergic response. 25 The literature shows that a decrease in cardiac β-receptor number has been reported in several hypertensive models known to be associated with an increase in sympathetic nerve activity, including SHR.…”

Section: Discussionmentioning

confidence: 99%

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Fasting/Refeeding Cycles Prevent Myocardial Dysfunction and Morphology Damage in the Spontaneously Hypertensive Rats

Pinotti

Matias

Sugizaki

et al. 2018

Arquivos Brasileiros De Cardiologia

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BackgroundCaloric restriction is known to impair the cardiac function and morphology in hypertrophied hearts of spontaneously hypertensive rats (SHR); however, the influence of fasting/refeeding (RF) is unknown.ObjectiveTo investigate the fasting/refeeding approach on myocardial remodeling and function. In addition, the current study was designed to bring information regarding the mechanisms underlying the participation of Ca2+ handling and β-adrenergic system.MethodsSixty-day-old male SHR rats were submitted to food ad libitum (C), 50% food restriction (R50) or RF cycles for 90 days. Cardiac remodeling was assessed by ultrastructure analysis and isolated papillary muscle function. The level of significance considered was 5% (α = 0.05).ResultsThe RF rats presented lower cardiac atrophy than R50 in relation to C rats. The C rats increased weight gain, R50 maintained their initial body weight and RF rats increased and decreased weight during RF. The RF did not cause functional impairment because the isotonic and isometric parameters showed similar behavior to those of C. The isotonic and isometric cardiac parameters were significantly elevated in RF rats compared to R50 rats. In addition, the R50 rats had cardiac damage in relation to C for isotonic and isometric variables. While the R50 rats showed focal changes in many muscle fibers, the RF rats displayed mild alterations, such as loss or disorganization of myofibrils.ConclusionFasting/refeeding promotes cardiac beneficial effects and attenuates myocardial injury caused by caloric restriction in SHR rats, contributing to reduce the cardiovascular risk profile and morphological injuries. Furthermore, RF promotes mild improvement in Ca2+ handling and β-adrenergic system.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Fasting/Refeeding Cycles Prevent Myocardial Dysfunction and Morphology Damage in the Spontaneously Hypertensive Rats

Pinotti

Matias

Sugizaki

et al. 2018

Arquivos Brasileiros De Cardiologia

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“…24,25 We observed that severe food restriction induces mild ultrastructural, morphological, and functional changes in normal rat hearts, which are exacerbated by hemodynamic overload in hypertensive rats. 32-37 Therefore, the occurrence of cachexia can further impair cardiac changes and heart failure in a fatal vicious cycle. Cachexia can also exacerbate heart failure-associated anemia and gastrointestinal changes.…”

Section: Clinical Consequences Of Cachexiamentioning

confidence: 99%

Cardiac Cachexia: Perspectives for Prevention and Treatment

Okoshi¹,

Capalbo²,

Romeiro³

et al. 2016

Arquivos Brasileiros De Cardiologia

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Cachexia is a prevalent pathological condition associated with chronic heart failure. Its occurrence predicts increased morbidity and mortality independent of important clinical variables such as age, ventricular function, or heart failure functional class. The clinical consequences of cachexia are dependent on both weight loss and systemic inflammation, which accompany cachexia development. Skeletal muscle wasting is an important component of cachexia; it often precedes cachexia development and predicts poor outcome in heart failure. Cachexia clinically affects several organs and systems. It is a multifactorial condition where underlying pathophysiological mechanisms are not completely understood making it difficult to develop specific prevention and treatment therapies. Preventive strategies have largely focused on muscle mass preservation. Different treatment options have been described, mostly in small clinical studies or experimental settings. These include nutritional support, neurohormonal blockade, reducing intestinal bacterial translocation, anemia and iron deficiency treatment, appetite stimulants, immunomodulatory agents, anabolic hormones, and physical exercise regimens. Currently, nonpharmacological therapy such as nutritional support and physical exercise are considered central to cachexia prevention and treatment.

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“…Left ventricular isolated papillary muscle preparations allow us to properly control preload and afterload and analyze intrinsic myocardial function without the effects of systemic metabolic changes [ 34 – 36 ]. Furthermore, by using positive inotropic stimulation, it is also possible to evaluate myocardial contractile reserve in papillary muscle preparations [ 37 , 38 ]. Therefore, in this study we evaluated the influence of a low intensity aerobic exercise protocol on in vivo cardiac remodeling and in vitro myocardial function in rats with streptozotocin-induced diabetes mellitus.…”

Section: Introductionmentioning

confidence: 99%

Low Intensity Physical Exercise Attenuates Cardiac Remodeling and Myocardial Oxidative Stress and Dysfunction in Diabetic Rats

Gimenes

Rosa

et al. 2015

Journal of Diabetes Research

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We evaluated the effects of a low intensity aerobic exercise protocol on cardiac remodeling and myocardial function in diabetic rats. Wistar rats were assigned into four groups: sedentary control (C-Sed), exercised control (C-Ex), sedentary diabetes (DM-Sed), and exercised diabetes (DM-Ex). Diabetes was induced by intraperitoneal injection of streptozotocin. Rats exercised for 9 weeks in treadmill at 11 m/min, 18 min/day. Myocardial function was evaluated in left ventricular (LV) papillary muscles and oxidative stress in LV tissue. Statistical analysis was given by ANOVA or Kruskal-Wallis. Echocardiogram showed diabetic groups with higher LV diastolic diameter-to-body weight ratio and lower posterior wall shortening velocity than controls. Left atrium diameter was lower in DM-Ex than DM-Sed (C-Sed: 5.73 ± 0.49; C-Ex: 5.67 ± 0.53; DM-Sed: 6.41 ± 0.54; DM-Ex: 5.81 ± 0.50 mm; P < 0.05 DM-Sed vs C-Sed and DM-Ex). Papillary muscle function was depressed in DM-Sed compared to C-Sed. Exercise attenuated this change in DM-Ex. Lipid hydroperoxide concentration was higher in DM-Sed than C-Sed and DM-Ex. Catalase and superoxide dismutase activities were lower in diabetics than controls and higher in DM-Ex than DM-Sed. Glutathione peroxidase activity was lower in DM-Sed than C-Sed and DM-Ex. Conclusion. Low intensity exercise attenuates left atrium dilation and myocardial oxidative stress and dysfunction in type 1 diabetic rats.

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Food restriction impairs myocardial inotropic response to calcium and β-adrenergic stimulation in spontaneously hypertensive rats

Cited by 7 publications

References 34 publications

Fasting/Refeeding Cycles Prevent Myocardial Dysfunction and Morphology Damage in the Spontaneously Hypertensive Rats

Fasting/Refeeding Cycles Prevent Myocardial Dysfunction and Morphology Damage in the Spontaneously Hypertensive Rats

Cardiac Cachexia: Perspectives for Prevention and Treatment

Low Intensity Physical Exercise Attenuates Cardiac Remodeling and Myocardial Oxidative Stress and Dysfunction in Diabetic Rats

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