Repeated high fat and high carbohydrate meals (HFHCM) generate atherosclerosis, isolated systolic hypertension
(ISH), autonomic and endothelial dysfunction. Consequently, old people are particularly susceptible to both flowmediated
dilation (FMD) impairment and postprandial hypotension. Despite the mounting evidence that free radicals substantially
alter blood pressure and endothelial function, the mechanisms that outline these phenomena are unclear. We
have reviewed the effects of the free radicals generated by post-prandial oxidative burst on vascular contractility. Postprandial
endotoxemia seems to play a crucial role in both oxidative burst and inflammatory response after meal. Oxidative
burst produces both reactive oxygen species (ROS) and reactive nitrogen species (RNS). The reviewed results do not support
the hypothesis that a sparing NO• effect is the primary cause of the early alteration of vascular contractility induced
by oxidative burst. The contrasting results of various ROS seem to be due to the differentiated effect or toxicity to endothelium
or vascular smooth muscle, while lypopolisaccaride, peroxinitrite and peroxyl radicals induce hypotension. On the
other hand, immune activation improves sympathetic nervous system (SNS) activity and the compensatory adrenergic response
to postprandial hypotension has anti-inflammatory activity. Besides, insulin inhibits post-prandial oxidative burst,
post-prandial oxidative stress and inflammation activate the xanthine oxidase and induce the antioxidant enzymes. In conclusion,
repeated HFHCM meal ingestion could induce hyper-insulinaemia, chronic SNS and antioxidant enzymes activation.
These defensive mechanisms, to both post-prandial hypotension and inflammation, generate autonomic dysfunction and FMD
impairment, whereas the chronic oxidative stress induces structural changes in the arteries leading to ISH.