Weight Gain–Induced Blood Pressure Elevation

Masuo, Kazuko; Mikami, Hiroshi; Ogihara, Toshio; Tuck, Michael L.

doi:10.1161/01.hyp.35.5.1135

Cited by 131 publications

(112 citation statements)

References 29 publications

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“…Only the subjects who had not changed their diet, exercise or body weight (45% provided in their biannual medical evaluation records) over the previous 6 months, including the run-in period of 1 month, were eligible for enrollment. 23,24 Randomization was stratified according to basal BP and body mass index (BMI). Average age at the baseline period was 38 ± 5 years for the diet alone group, 37±6 years for exercise alone group and 38±5 years for the combination of diet and exercise group.…”

Section: Methods Subjectsmentioning

confidence: 99%

Different mechanisms in weight loss-induced blood pressure reduction between a calorie-restricted diet and exercise

et al. 2011

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The present study compared the effectiveness of a mild calorie-restricted diet (D) alone, exercise (EX) alone and a combination of D+EX on weight loss-induced blood pressure (BP) reduction over 24 weeks. We focussed especially on the relationship between sympathetic nervous activity, as indicated from measures of plasma norepinephrine (NE), and insulin resistance (homeostasis model of insulin resistance, HOMA-IR). The three groups each comprised 30 obese, hypertensive men. Body mass index (BMI), fat mass, waist-to-hip ratio, BP, plasma NE and HOMA-IR were measured every 2 weeks during the first 4 weeks and subsequently every 4 weeks for the next 20 weeks. All basal parameters were similar among the three groups. At 24 weeks, the combination group with D+EX comprised a significantly higher prevalence of normotensive subjects than the D alone or EX alone group (Po0.05). In the D alone group, plasma NE was decreased significantly at 2 weeks, reductions in BMI, fat mass and BP were observed at 8 weeks, and waist-to-hip ratios and HOMA-IR were decreased at 12 weeks. In comparison, in the EX alone group, significant reductions of fat mass and HOMA-IR were observed at 4 weeks. Plasma NE and HOMA-IR were reduced at 8 weeks while decreases in BP were detected at 12 weeks. In the D+EX group, significant reductions in plasma NE were observed at 2 weeks followed by significant decreases in BMI, fat mass, waist-to-hip ratio, BP levels and HOMA-IR at 4 weeks. The magnitudes of reductions of all parameters were greatest in the D+EX group. These results demonstrate that D+EX exerts a stronger ameliorative effect on weight loss, weight loss-induced BP reduction, normalization of BP, sympathetic activation and insulin resistance compared with D or EX alone. D and EX might, perhaps, exert different mechanisms on weight loss and weight loss-induced BP reduction; however, a combination of caloric restriction and exercise is preferred to control BP levels in obese hypertensive patients.

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Section: Methods Subjectsmentioning

confidence: 99%

Different mechanisms in weight loss-induced blood pressure reduction between a calorie-restricted diet and exercise

et al. 2011

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“…Only subjects whose body weight had not changed for at least the previous 1 year (weight change o5% provided in their biannual medical evaluation records) were enrolled in the present study. 17,29 The protocol was approved by the ethics committee of Osaka University Graduate School of Medicine, Japan, and written informed consent was obtained from all the subjects.…”

Section: Methods Subjectsmentioning

confidence: 99%

“…In many clinical and epidemiological studies, elevated sympathetic nervous activity has been documented in obesity 16 or weight gain [17][18][19] and in patients with end-stage renal disease. 7,[20][21][22] Zoccali et al 20,22 reported that the degree of sympathetic nervous activation might relate to the occurrence of fatal cardiovascular events.…”

Section: Introductionmentioning

confidence: 99%

Effects of weight loss on renal function in overweight Japanese men

et al. 2011

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Obesity is known as an independent risk factor for renal injury. Sympathetic nerve activation may have an important role of the pathogenesis of obesity, and hypertension may underpin the development of cardiovascular events. In the present study, we evaluated the effects of weight loss (WL) on renal function, especially focusing on sympathetic nervous activity. In 154 overweight or obese Japanese men (89 normotensive and 65 untreated mild hypertensive subjects), body weight, body mass index (BMI), total body fat mass, blood pressure (BP), serum creatinine, blood urea nitrogen, creatinine clearance (CCr) (calculated with the Cockcroft-Gault equation) and plasma norepinephrine (NE) were measured before and after a 12-month period of WL with a mild caloric-restricted diet and exercise. A significant WL was defined as 10% or more WL compared with the entry period. In total, 97 (63.0%) subjects succeeded in significant (by 14.3%) WL at 12 months, and 57 subjects (37.0%) did not succeed in significant WL but they lost 7.7% weight. At entry, levels of plasma NE, serum creatinine and fat mass were significantly lower and CCr was greater in the group with a significant WL compared with those without WL. BMI, total body fat mass and plasma NE significantly decreased, and CCr increased with WL. At both baseline and at the 12-month period, fat mass and plasma NE negatively correlated with CCr and positively correlated with creatinine at each time point. Changes in fat mass and plasma NE over 12 months correlated with changes in creatinine, and only changes in fat mass negatively correlated with changes in CCr. Basal fat mass and plasma NE correlated positively with serum creatinine at 12 months and negatively with CCr at the same time point. In multiple regression analyses, basal plasma NE and fat mass were significant determinants of serum creatinine levels and CCr at 12 months.In conclusion, WL improved renal function (as evident from measures of creatinine and CCr) in overweight individuals. Basal plasma NE levels and total body fat mass could be predictors for improvement in renal function associated with WL. Suppression of sympathetic nervous activation associated with WL may have a role in the ameliorative effects on renal function.

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“…Finally, insulin resistance has also been exhibited as an effect of heightened sympathetic drive, through b-adrenergic stimulation and/or vasoconstriction with subsequent reduction of muscular blood flow. 45,46 Leptin and neuropeptides Hyperleptinemia is another possible link between obesity and the development of hypertension. Leptin is a peptide hormone secreted from adipose tissue in direct proportion to adipose tissue mass.…”

Section: Function Of Hormones Insulinmentioning

confidence: 99%

Mechanisms of obesity-induced hypertension

et al. 2010

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The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi:10.1038/hr.2010.9Keywords: leptin; obesity; pressure natriuresis; rennin-angiotensin-aldosterone system; sympathetic nervous system INTRODUCTION Obesity is a common disorder that develops from the interaction between the genotype and the environment and involves social, behavioral, cultural, physiological, metabolic and genetic factors. A large number of studies have shown that obesity has an important negative impact on health in a population, leading to the recommendation for general practitioners to have an important function in the management of this condition and of its associated comorbidities such as hypertension, hyperlipidemia and hyperinsulinemia/insulin resistance. The relationship between obesity and hypertension is well established both in adults and children. 1,2 Obese individuals exhibit higher levels of office as well as ambulatory blood pressure (BP) from childhood to old age. Obese subjects display higher BP levels than non-obese individuals even in the normotensive range. The combination of obesity, hypertension and other cardiovascular risk factors significantly increases the probability of adverse cardiovascular outcomes, and raises considerations for aggressive treatment strategies. 3 The mechanisms through which obesity directly causes hypertension are still an area of research. Human and animal studies have elucidated the function of adipose tissue derivatives (adipokines and cytokines), neurohumoral pathways, metabolic functions and modulation of pressor/depressor mechanisms. Although obesity-related hypertension may be the result of a combinatio...

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Weight Gain–Induced Blood Pressure Elevation

Cited by 131 publications

References 29 publications

Different mechanisms in weight loss-induced blood pressure reduction between a calorie-restricted diet and exercise

Different mechanisms in weight loss-induced blood pressure reduction between a calorie-restricted diet and exercise

Effects of weight loss on renal function in overweight Japanese men

Mechanisms of obesity-induced hypertension

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