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The sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension
S E Kjeldsen1, M Rostrup, A Moan
1Department of Internal Medicine, Ullevål University Hospital, Oslo, Norway.
Insights
The sympathetic nervous system may link stress and cardiovascular disease by causing metabolic syndrome in hypertensive individuals. Elevated catecholamines contribute to high blood pressure and atherogenic biochemical abnormalities.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Neuroscience
Background:
- Hypertension is associated with coronary artery disease.
- Metabolic cardiovascular syndrome involves atherogenic biochemical abnormalities.
- Sympathetic nervous system overactivity is reported in hypertensive subjects.
Purpose of the Study:
- To explore the role of the sympathetic nervous system in metabolic cardiovascular syndrome.
- To investigate the link between catecholamines, metabolic abnormalities, and hypertension.
- To understand the connection between stress and cardiovascular disease via the sympathetic nervous system.
Main Methods:
- Review of existing literature on sympathetic nervous system activity, catecholamines, and metabolic syndrome in hypertension.
- Analysis of the hormonal effects of plasma catecholamines.
- Examination of evidence linking epinephrine to blood platelet dysfunction.
Main Results:
- Elevated plasma catecholamines can cause metabolic cardiovascular syndrome.
- Catecholamines increase total cholesterol, triglycerides, and insulin, while decreasing HDL cholesterol.
- Sympathetic nervous system overactivity may modulate metabolic syndrome in essential hypertension.
Conclusions:
- The sympathetic nervous system plays a crucial role in the metabolic cardiovascular syndrome associated with hypertension.
- Catecholamine-induced metabolic hormonal effects may be the link between stress and cardiovascular disease.
- Hypertensive individuals may exhibit exaggerated sympathoadrenal responses to stimuli.
Abstract:
The association between blood pressure and coronary artery disease may be caused by a concurrence of atherogenic biochemical abnormalities in hypertensive patients, i.e., the metabolic cardiovascular syndrome (increased total cholesterol, triglycerides, and insulin; decreased high-density lipoprotein (HDL) cholesterol; and insulin resistance, glucose intolerance, and blood platelet dysfunction). There are numerous reports of sympathetic nervous system overactivity in hypertensive subjects that could be of importance for the pathophysiology of the high blood pressure. Plasma catecholamines have metabolic hormonal effects at concentrations slightly above low normal resting levels. Even transiently and certainly chronically raised plasma catecholamine levels may cause biochemical abnormalities. Catecholamines may raise total cholesterol, triglycerides, and insulin, decrease HDL cholesterol, and cause insulin resistance and glucose intolerance, and recent evidence supports an in vivo influence of epinephrine on blood platelets, causing dysfunction in hypertensive subjects. Thus, the sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension. Hypertensive subjects may respond to environmental stimuli with larger sympathoadrenal responses than normal subjects. Furthermore, emotional stress has been associated with coronary artery disease. Thus, the metabolic hormonal effects of catecholamines, by causing the metabolic cardiovascular syndrome, may be the crucial link between "stress" and cardiovascular disease.