title: The sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension.
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.
authors.affiliation: Department of Internal Medicine, Ullevål University Hospital, Oslo, Norway.
authors.forename: S E
authors.initials: SE
authors.lastname: Kjeldsen
authors.forename: M
authors.initials: M
authors.lastname: Rostrup
authors.forename: A
authors.initials: A
authors.lastname: Moan
authors.forename: H H
authors.initials: HH
authors.lastname: Mundal
authors.forename: K
authors.initials: K
authors.lastname: Gjesdal
authors.forename: I K
authors.initials: IK
authors.lastname: Eide
mesh_terms: D001792:Blood Platelets / Q000502:physiology; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D002395:Catecholamines / Q000097:blood; D003327:Coronary Disease / Q000503:physiopathology*; D005951:Glucose Tolerance Test; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008659:Metabolic Diseases / Q000503:physiopathology*; D012307:Risk Factors; D013564:Sympathetic Nervous System / Q000502:physiology*; D013577:Syndrome
chemical_list: D002395:Catecholamines; D008055:Lipids