Name: CAMILA ALMENARA CRUZ PEREIRA

Publication date: 30/03/2017
Advisor:

Namesort descending Role
ALESSANDRA SIMAO PADILHA Advisor *

Examining board:

Namesort descending Role
AGATA LAGES GAVA Internal Examiner *
ALESSANDRA SIMAO PADILHA Advisor *
MARCELO PERIM BALDO External Examiner *
ROGER LYRIO DOS SANTOS Internal Examiner *

Summary: It has been already described that fructose can acutely interferes on cardiovascular function in humans and in animals, but the mechanisms underlying this effect remain unclear. Thus, we sought to test whether fructose can affect the vascular function without the interference of its metabolic effect. We exposed aortic segments from Wistar rats to 4, 20 or 40 mM of fructose or mannitol for 30 minutes and then evaluated
the vascular responses to vasoactive agents. We also analyzed oxygen consumption by cultured endothelial cells after fructose supplementation (1 and 10 mM). Fructose increased the response to phenylephrine and reduced endothelium dependent relaxation elicited by acetylcholine, but did not change vascular responses to sodium nitroprusside. Fructose also reduced the contractile responses to phenylephrine of endothelium denuded and L-NAME incubated aorta. SOD and apocynin increased the
response to acetylcholine only on fructose exposed-vessels. Additionally, SOD, apocynin and catalase reduced the contractile response induced by phenylephrine more in fructose exposed-aortic rings. Moreover, catalase reduced vascular response to acetylcholine only on mannitol-exposed aorta. Finally, fructose addition did not affect the basal oxygen consumption rate, the proton leakage and the maximal respiratory
capacity on endothelial cells. Our results demonstrated that acute fructose exposure increases superoxide anion produced by NADPH oxidase and, consequently, increases NO degradation. Also, the enhanced vasoconstrictor action of hydrogen peroxide might contribute to exacerbated contractile responses. This vasoactive imbalance might be the key role by which fructose induces an acute vasoconstrictor
response and can explain the vascular alterations observed after fructose ingestion.

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