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Updated: Aug 29, 2026

Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats
Published on: September 11, 2018
Abdominal fat and sympathetic overactivity. From calorie intake to postmenopausal hypertension
1Molecular Cardiology Laboratory, Department of Internal Medicine and Cardiology, Philipps University Marburg, Germany. Rupp@staff.uni-marburg.de
Background:
Epidemiologic studies have found an association between overweight and increased mortality arising primarily from cardiovascular disorders. A major determinant is a chronically raised sympathetic nervous system activity which can arise from calorie intake-dependent and -independent mechanisms. Calorie-dependent parameters reflecting sympathetic overactivity are an increased body fat mass and body mass index.
Visceral Fat:
Although influenced by calorie intake to a certain extent, visceral fat accumulation is a mechanism which is determined also by estrogen deficiency (postmenopausal hypertension) or enhanced corticoid influences. It is hypothesized that excess catecholamines trigger various adverse processes which, if they persist, can lead or aggravate hypertension and insulin resistance. Visceral but not peripheral fat mass was correlated with atherogenic metabolites.
Excess Catecholamine Syndrome:
The present focus on visceral fat accumulation strengthens the concept of an "excess catecholamine syndrome" of which the "metabolic syndrome" appears as one consequence. It is proposed to further assess the potential of transthoracic echocardiography as routine imaging method for the prediction of visceral fat accumulation and its adverse health consequences.
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