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Under some pathophysiological circumstances, endothelium-derived vasoconstricting factors, such as ET-1, AT-II, urotensin II, superoxide anions, vasoconstrictor prostaglandins and thromboxane A 2 , can be released and contribute to the paradoxical vasoconstrictor effects

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This hypothesis is further supported by clinical observations that more than 60% of accumulated fatty acids in the liver are derived from the circulation in NAFLD patients 7,8