Sympathetic and Renin-Angiotensin Systems Contribute to Increased Blood Pressure in Sucrose-Fed Rats

Freitas, Raphael Ribeiro de Aquino; Lopes, Karen Lucasechi; Carillo, Bruno A.; Bergamaschi, Cássia T.; Carmona, Adriana K.; Casarini, Dulce Elena; Furukawa, Luzia Naôko Shinohara; Heimann, Joel Cláudio; Campos, Rui; Dolnikoff, Miriam Sterman

doi:10.1016/j.amjhyper.2007.01.014

Cited by 17 publications

(12 citation statements)

References 28 publications

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“…These findings contrast with previous reports of cardiomyocyte contractile dysfunction in sucrose-fed mice (12,49) and may reflect the different systemic and cardiovascular phenotype induced by sucrose and fructose diets. High sucrose diets have been reported to induce hyperinsulinemia and hypertension with normal glucose levels (12,15,49), whereas the fructosefed mouse model employed in the present study exhibits normal insulin levels, hyperglycemia, and no change in blood pressure (35).…”

Section: Camentioning

confidence: 75%

Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca²⁺handling and myofilament responsiveness

Mellor¹,

Wendt

Ritchie

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Mellor KM, Wendt IR, Ritchie RH, Delbridge LM. Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca 2ϩ handling and myofilament responsiveness. Am J Physiol Heart Circ Physiol 302: H964 -H972, 2012. First published December 23, 2011; doi:10.1152/ajpheart.00797.2011.-High fructose intake has been linked to insulin resistance and cardiac pathology. Dietary fructose-induced myocardial signaling and morphological alterations have been described, but whether cardiomyocyte function is influenced by chronic high fructose intake is yet to be elucidated. The goal of this study was to evaluate the cardiomyocyte excitationcontraction coupling effects of high dietary fructose and determine the capacity for murine cardiomyocyte fructose transport. Male C57Bl/6J mice were fed a high fructose diet for 12 wk. Fructose-and controlfed mouse cardiomyocytes were isolated and loaded with the fura 2 ) was reduced, and protein phosphatase 2A expression increased, in fructosefed mouse hearts. Hypertension and cardiac hypertrophy were not evident. These findings demonstrate that fructose diet-associated myocardial insulin resistance induces profound disturbance of cardiomyocyte Ca 2ϩ handling and responsiveness in the absence of altered systemic loading conditions. excitation-contraction coupling; cardiac; myocardial; cellular IN WESTERN SOCIETIES, the use of added sweeteners has increased by 25% during the last 30 years, and it has been estimated that the average adolescent (North American) consumes over 30% of energy intake in the form of added sugars (17,29). Fructose intake has been identified as a significant risk factor for insulin resistance and cardiovascular disease, independent of body mass index (45). Experimental models have demonstrated that a high fructose diet disturbs metabolic homeostasis, increases plasma fructose, and induces systemic insulin resistance in rodents (2,24,32,35). The existence of an insulin-resistant cardiomyopathy, associated with perturbed cardiac metabolism and functional impairment, is generally recognized (33,46,48). In a previous study, we have demonstrated that excess fructose intake is associated with elevated blood glucose, glucose intolerance, and normal plasma insulin in the absence of hypertension and obesity (35). We have also shown that fructose feeding induces diffuse myocardial fibrotic infiltration linked with suppressed cardiomyocyte viability signaling (35). The impact of elevated dietary fructose intake on cardiomyocyte functional performance is yet to be demonstrated.Cellular fructose uptake is mediated by insulin-independent transporters. Fructose is rapidly phosphorylated by fructokinase and bypasses the glycolytic rate-limiting enzyme, phosphofructokinase, proceeding through glycolysis to produce pyruvate and lactate in a less-controlled manner than glucose (30). The close association of glycolytic enzymes with Ca 2ϩ -related transporters provides indication that specific excitationcontraction coupling processes are particularly reliant on glycolyt...

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Section: Camentioning

confidence: 75%

Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca²⁺handling and myofilament responsiveness

Mellor¹,

Wendt

Ritchie

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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show abstract

“…Alterations of the rennin-angiotensin-aldosterone system (RAAS) have also been suggested for the cardiovascular changes in response to chronic sucrose feeding (Giacchetti et al, 2000;Freitas et al, 2007), and many findings even have shown overexpression of angiotensin type 1 (AT 1 ) receptor, a kind of G-protein-coupled receptors, and activation of renal and heart RAAS as potential mechanisms (Giacchetti et al, 2000;Freitas et al, 2007). In fact, angiotensin receptor blockers and angiotensin converting enzyme inhibitors were shown to decrease the elevated SBP in fructose-fed or essential hypertensive rats (Limura et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Antihypertensive effect of total flavones extracted from seed residues of Hippophae rhamnoides L. in sucrose-fed rats

Pang

Zhao

Wen

et al. 2008

Journal of Ethnopharmacology

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“…However, peripheral vascular resistance in the fructose drinking group increased significantly [ 37 ]. In another study [ 38 ], metabolic syndrome was formed by giving 23% glucose, fructose, and sucrose within drinking water during 14 days. The animals were found with equal amounts of water to drink fructose-drinking group compared to the control animals.…”

Section: Discussionmentioning

confidence: 99%

Effect of Caffeic Acid Phenethyl Ester on Vascular Damage Caused by Consumption of High Fructose Corn Syrup in Rats

Gun

Özer

Bilğiç

et al. 2016

Oxidative Medicine and Cellular Longevity

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Fructose corn syrup is cheap sweetener and prolongs the shelf life of products, but fructose intake causes hyperinsulinemia, hypertriglyceridemia, and hypertension. All of them are referred to as metabolic syndrome and they are risk factors for cardiovascular diseases. Hence, the harmful effects of increased fructose intake on health and their prevention should take greater consideration. Caffeic Acid Phenethyl Ester (CAPE) has beneficial effects on metabolic syndrome and vascular function which is important in the prevention of cardiovascular disease. However, there are no known studies about the effect of CAPE on fructose-induced vascular dysfunction. In this study, we examined the effect of CAPE on vascular dysfunction due to high fructose corn syrup (HFCS). HFCS (6 weeks, 30% fed with drinking water) caused vascular dysfunction, but treatment with CAPE (50 micromol/kg i.p. for the last two weeks) effectively restored this problem. Additionally, hypertension in HFCS-fed rats was also decreased in CAPE supplemented rats. CAPE supplements lowered HFCS consumption-induced raise in blood glucose, homocysteine, and cholesterol levels. The aorta tissue endothelial nitric oxide synthase (eNOS) production was decreased in rats given HFCS and in contrast CAPE supplementation efficiently increased its production. The presented results showed that HFCS-induced cardiovascular abnormalities could be prevented by CAPE treatment.

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Sympathetic and Renin-Angiotensin Systems Contribute to Increased Blood Pressure in Sucrose-Fed Rats

Abstract: These findings suggest a specific renal renin-angiotensin-sympathetic activation as a potential mechanism for the cardiovascular changes in response to chronic sucrose feeding.

Cited by 17 publications

References 28 publications

Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca²⁺handling and myofilament responsiveness

Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca²⁺handling and myofilament responsiveness

Antihypertensive effect of total flavones extracted from seed residues of Hippophae rhamnoides L. in sucrose-fed rats

Effect of Caffeic Acid Phenethyl Ester on Vascular Damage Caused by Consumption of High Fructose Corn Syrup in Rats

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Sympathetic and Renin-Angiotensin Systems Contribute to Increased Blood Pressure in Sucrose-Fed Rats

Abstract: These findings suggest a specific renal renin-angiotensin-sympathetic activation as a potential mechanism for the cardiovascular changes in response to chronic sucrose feeding.

Cited by 17 publications

References 28 publications

Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca2+handling and myofilament responsiveness

Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca2+handling and myofilament responsiveness

Antihypertensive effect of total flavones extracted from seed residues of Hippophae rhamnoides L. in sucrose-fed rats

Effect of Caffeic Acid Phenethyl Ester on Vascular Damage Caused by Consumption of High Fructose Corn Syrup in Rats

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Product

Resources

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Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca²⁺handling and myofilament responsiveness

Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca²⁺handling and myofilament responsiveness