Abstract
Introduction: During atherosclerosis process, vasoconstriction phenomenon occurs which in turn leads to tissue hypoxia. A few studies have been performed on the combination of atherosclerosis and hypoxia as stressors that may accelerate secretion of constrictors. The aim of present study was to evaluate the effects of atherosclerosis and hypoxia on serum levels of main vasoconstrictors (epinephrine, norepinephrine and renin). Methods: In this interventional study, 32 New Zealand white rabbits were randomly divided into four groups (n = 8): normal diet (control group), normal diet exposed to hypoxia (11%, 10 days), high-fat diet (cholesterol-2%, 8 weeks), and high-fat diet with hypoxia. Later, serum levels of renin, epinephrine and norepinephrine were measured on second, 56th and 66th days. Results: High-fat diet and hypoxia caused significant increase in epinephrine and norepinephrine concentrations on days 56 and 66 compared to the control group (P < 0.05). Also, renin showed significance increase in high-fat diet and high-fat diet+ hypoxia groups compared to the control group (P < 0.05). Conclusion: Both high-fat diet and hypoxia increase renin levels in male rabbits. Furthermore, the combination of high-fat diet and hypoxia immensely increases renin levels. Both hypoxia and combined of high-fat diet and hypoxia increase norepinephrine levels. However epinephrine is only increased in the combination of high-fat diet and hypoxia. So the presence of hypoxia in combination with high-fat diet, cause accelerated and aggravated atherosclerosis.
Highlights
During atherosclerosis process, vasoconstriction phenomenon occurs which in turn leads to tissue hypoxia
The present study was conducted to evaluate the effects of atherosclerosis and hypoxia on blood content of vasoconstrictors levels of epinephrine, norepinephrine and renin
Effect of hypoxia and high-fat diet on lipid profile Our results clearly demonstrated that 8 weeks consumption of 2% cholesterol diet significantly increased serum total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and TG
Summary
Atherosclerosis is the leading cause of mortality in the developed world. Atherosclerosis syndrome affecting arterial blood vessels. Fatty streak evolve to fibrous plaque and unstable plaque.[3] Vasoconstrictors including epinephrine, norepinephrine and renin-angiotensin are the key mechanical forces that affect the blood flow and stability of atherosclerotic plaques.[4] Activation of the renin-angiotensin system has different effects on cardiovascular system activity such as vasoconstriction and release of thromboxane A2.5 Blood vasoconstrictors, in long term, can cause high blood pressure, cardiac and vascular hypertrophy and progression of atherosclerotic plaques.[2] Some Studies have demonstrated that treatment with inhibitors of angiotensin-converting enzyme (ACEI) significantly reduced the incidence of myocardial attacks.[6,7] Laboratory studies, similar to experimental findings, have shown that use of angiotensin antagonists, reduced the risk of atherosclerosis.[8] Some researchers have suggested that angiotensin has a direct effect on vascular wall through an intracellular mechanism.[9] Unlike the known effects of angiotensin in atherosclerosis development, effects of catecholamines are different in ischemic and normal conditions.[10,11] Activity of vasoconstrictor system increases following hypoxia in order to increase the cardiac output and compensate the oxygen deficiency.[12] It was reported that elevated levels of catecholamines attributed to the hypertension in some conditions such as sleep apnea.[13] Studies have shown that atherosclerosis is a process in which vasoconstriction occurs; this in turn leads to tissue hypoxia. The present study was conducted to evaluate the effects of atherosclerosis and hypoxia on blood content of vasoconstrictors levels of epinephrine, norepinephrine and renin
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