The relation of adiposity to blood pressure and development of hypertension. The Framingham study.

Annals of internal medicine (Impact Factor: 16.1). 08/1967; 67(1):48-59.
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    ABSTRACT: Oxidative stress and the mineralocorticoid receptor (MR) are implicated in the pathogenesis of salt-induced left ventricular (LV) diastolic dysfunction associated with metabolic syndrome (MetS). We recently characterized DahlS.Z-Lepr(fa) /Lepr(fa) (DS/obese) rats, derived from a cross between Dahl salt-sensitive and Zucker rats, as a new animal model of MetS. We investigated the pathophysiological roles of increased oxidative stress and MR activation in cardiac injury with this model. DS/obese rats were treated with the antioxidant tempol (1 mmol/L in drinking water) or the selective MR antagonist eplerenone (15 mg/kg per day, per os) for 5 weeks beginning at 10 weeks of age. The increased systolic blood pressure and LV hypertrophy that develop in untreated DS/obese rats were substantially ameliorated by eplerenone but not by tempol. Eplerenone also attenuated LV fibrosis and diastolic dysfunction more effectively than did tempol in DS/obese rats, whereas cardiac oxidative stress and inflammation were reduced similarly by both drugs. Both the ratio of plasma aldosterone concentration to plasma renin activity and cardiac expression of the MR and serum/glucocorticoid-regulated kinase 1 genes were decreased to a greater extent by eplerenone than by tempol. Our results indicate that both increased oxidative stress and MR activation in the heart may contribute to the development of LV remodeling and diastolic dysfunction in DS/obese rats. The superior cardioprotective action of eplerenone is likely attributable to its greater antihypertensive effect, which is likely related to its greater inhibition of aldosterone-MR activity in the cardiovascular system.
    Nagoya journal of medical science 02/2015; 77(1-2):275-89. · 0.80 Impact Factor
  • Revista Colombiana de Cardiologia 02/2012; 19(2):75-79. DOI:10.1016/S0120-5633(12)70109-2
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    ABSTRACT: Background: Obesity induces oxidative stress and inflammation, which may lead to arterial stiffness and hypertension. The relationship of white blood cell count (WBC) and anthropometric indices with arterial stiffness index (ASI) and blood pressure was evaluated in this study. Methods: Thirty male subjects aged between 35-55 years were selected in each of normotensive, prehypertensive and hypertensive groups. Their weight, height, waist circumference (WC) and hip circumference (HC) were measured according to the WHO guidelines. BMI, waist hip ratio (WHR), waist stature ratio (WSR) and conicity index (CI) were calculated. ASI was calculated from digital volume pulse recorded by photoplethysmography with iWorx-214 physiological interface system. The white blood cell count and differential was done. One way ANOVA followed by Post Hoc Tukey's Test was applied to determine the difference between the groups. Pearson's coefficient was calculated to study the correlation. Statistically, p value < 0.05 was considered significant. Results: There was statistically significant difference in WHR (0.000), WC (0.003) and ASI (0.000) between the study groups but not BMI (0.223). Amongst the anthropometric measurements, WHR and WC had positive correlation with the systolic and diastolic blood pressure. The WBC and absolute neutrophil count correlated significantly with WHR and WC but not with ASI and blood pressure. Conclusions: The central obesity is a more robust risk factor for arterial stiffness and blood pressure than BMI. The inflammation may be involved in pathogenesis of visceral obesity and arterial stiffness that may be determined by elevated white blood cell counts.