Obesity and hypertension.

This article has discussed some of the mechanisms involved in the causal relation between obesity and hypertension. Obesity causes a constellation of maladaptive disorders that individually and synergistically contribute to hypertension, among other cardiovascular morbidities. Well-designed population-based studies are needed to assess the individual contribution of each of these disorders to the development of hypertension. In addition, because the control of obesity may eliminate 48% of the hypertension in whites and 28% in blacks, this article has offered an up-to-date on the management of this problem. It is hoped that this article will help scientists formulate a thorough understanding of obesity hypertension and form the basis for more research in this field, which has a huge impact on human life.     

Obesity and arterial hypertension

Obesity is an independent risk factor for the development and progression of hypertension, cardiovascular disease and chronic kidney disease. There is growing evidence that obesity and associated metabolic abnormalities may induce and accelerate renal complications in essential hypertension. The clustering of obesity and other features of the metabolic syndrome might have important implications for prevention, particularly with regard to whether interventions targeted at visceral obesity would have beneficial effects on cardiovascular and renal morbidity.     

Obesity and hypertension in blacks

In the United States, obesity and hypertension are more common in blacks than in whites, but that general statement hides some important sex differences. Thus, in black women the prevalences of both obesity and hypertension are greater than in white women, whereas in men, although there is no racial difference in obesity, in blacks hypertension is more common and more severe than in whites. For white people, there is a well-documented causal relationship between obesity and hypertension, however, results from the second National Health and Nutrition Examination (NHANES II) suggest that this relationship is not so strong for blacks. Obesity is also an important risk factor for diabetes, which in itelf is associated with hypertension. The mechanisms of obesity-associated hypertension appears to be an inadequate vasodilation in the face of the increased blood volume and cardiac output, which are the natural consequences of an increased body mass. This defect in control of vascular resistance has been attributed to increased activity of the sympathetic nervous system, abnormal reninangiotensin-aldosterone relationships, and insulin resistance. However, none of these attributes has been found to be the exclusive characteristic of obese hypertensive as compared with normotensive obese subjects.     

Obesity, hypertension and insulin resistance

Being overweight or obese has become highly prevalent in Western countries and are rapidly reaching epidemic proportions in the developing world. Obesity-related disorders, such as hypertension and diabetes, are also increasing at an alarming rate. The relationship between obesity, hypertension and insulin resistance is well recognised, but the molecular mechanisms involved remain relatively poorly understood. Adipose tissue plays a key role in the pathogenesis of the metabolic syndrome. It serves as an important source of pro-inflammatory molecules, including leptin, tumour necrosis factor alpha, angiotensin II and interleukin-6, as well as anti-inflammatory molecules, such as adiponectin. Knowledge of how these adipose tissue-derived factors influence metabolic and cardiovascular disease has recently expanded. Leptin is now considered to play a key role in the elevation of sympathetic activity commonly found in obese, hypertensive patients, and decreased secretion of adiponectin appears to be an important predictor of diabetes. The ectopic storage of excess fat in skeletal muscle, liver or pancreas, due to the decreased capacity of adipose tissue to scavenge excess calories, may also play a role in the development of insulin resistance and type 2 diabetes. Overall, continuing research into the relationship between adipose-tissue biology and metabolic abnormalities may lead to a better understanding of the molecular mechanisms underlying the relationship between obesity and cardiovascular disease, and ultimately provide alternative treatments for the control of potentially life-threatening conditions.     

Obesity, hypertension and the metabolic syndrome

The prevalence of obesity in both developed and developing countries has increased dramatically in recent years.1Many people who are obese develop metabolic changes that increase the risk of diabetes mellitus and adverse cardiovascular outcomes. Obesity leads to the development of insulin resistance, lipid abnormalities and increased blood pressure.……     

Obesity,hypertension and home sphygmomanometer cuffs

BackgroundSince the increasing prevalence of obesity leads to a larger mean arm circumferences in the hypertensive population and appropriate cuff size is essential for accurate measurement of blood pressure, overweight and obese patients often require automated home sphygmomanometers with large- or extra large-sized cuffs. The aims of this study were to evaluate the information about cuff size on automated upper arm home sphygmomanometer packing boxes and compare the findings with wrist device boxes.MethodsOne hundred twelve different device boxes (49 automated upper arm, 5 semi-automatic, and 58 wrist) produced by 40 manufacturers were investigated.ResultsThree different types of information were observed (written, graphical, or a combination of both). There was not any information about cuff size on 49 (44%) device boxes. Most of the information expressed on the boxes was not attractive or informative for the patients.ConclusionThis study showed that the information regarding cuff size on most of the device boxes was obtuse and the patients are not warned sufficiently about appropriate cuff size. Physicians and health care providers should inform and train their patients about appropriate cuff size.     

Obesity, hypertension, and vascular disease

Obesity, hypertension, and related metabolic and hemodynamic abnormalities contribute significantly to cardiovascular disease in westernized societies such as the United States. Both obesity and hypertension are more prevalent among minorities such as black and Hispanic populations. Obesity substantially increases the likelihood of hypertension, and weight reduction has been shown to be an effective hygienic measure in reducing blood pressure. There is accumulating evidence that central obesity, particularly obesity that is distributed in the paraomental (visceral) region, especially predisposes one to hypertension and related metabolic abnormalities that contribute cerebrovascular disease.     

Obesity, hypertension, and the heart

Controversy exists regarding the amount of risk caused by obesity, but there is general consensus that it is associated with many serious disorders, mostly cardiovascular and neoplastic. Obesity is clearly associated with hypertension, ventricular remodeling with subsequent congestive heart failure, sleep-disordered breathing, and sudden death. The physiologic alterations associated with establishing and perpetuating the obese state are complex but are becoming clear. In discussing the cardiovascular consequences of obesity, the implications and mechanism of the associated hypertension need to be understood. There is growing recognition that adipose tissue is a very active in the neurohormonal axis and is not simply a passive storage depot. Among other things, adipocyte-related hormonal activity and resistance to feedback mechanisms are associated with increased plasma volume and increased sympathetic tone.     

Obesity, sleep apnea, and hypertension

Obesity has a high and rising prevalence and represents a major public health problem. Obstructive sleep apnea (OSA) is also common, affecting an estimated 15 million Americans, with a prevalence that is probably also rising as a consequence of increasing obesity. Epidemiologic data support a link between obesity and hypertension as well as between OSA and hypertension. For example, untreated OSA predisposes to an increased risk of new hypertension, and treatment of OSA lowers blood pressure, even during the daytime. Possible mechanisms whereby OSA may contribute to hypertension in obese individuals include sympathetic activation, hyperleptinemia, insulin resistance, elevated angiotensin II and aldosterone levels, oxidative and inflammatory stress, endothelial dysfunction, impaired baroreflex function, and perhaps by effects on renal function. The coexistence of OSA and obesity may have more widespread implications for cardiovascular control and dysfunction in obese individuals and may contribute to some of the clustering of abnormalities broadly defined as the metabolic syndrome. From the clinical and therapeutic perspectives, the presence of resistant hypertension and the absence of a nocturnal decrease in blood pressure in obese individuals should prompt the clinician to consider the diagnosis of OSA, especially if clinical symptoms suggestive of OSA (such as poor sleep quality, witnessed apnea, excessive daytime somnolence, and so forth) are also present.     

Obesity, hypertension, and the heart

Hypertension occurs more commonly in obese than in lean persons at virtually every age. A variety of endocrine, genetic, and metabolic mechanisms have been linked to the development of obesity hypertension. These include insulin resistance and hyperinsulinemia, increased serum aldosterone levels, salt sensitivity and expanded plasma volume in the presence of increased peripheral vascular resistance, a genetic predisposition, and possibly increased leptin levels. Pressure and volume overload are present in obese hypertensives. This leads to a mixed eccentric-concentric form of left ventricular hypertrophy and increases the predisposition to congestive heart failure. Weight loss, even in modest decrements, is effective in reducing obesity-hypertension, possibly by ameliorating several of the proposed pathophysiologic mechanisms. There are currently no specific recommendations concerning pharmacotherapy of obesity-hypertension because each drug group has pros and cons.     

Obesity and hypertension: from pathophysiology to treatment

While the prevalence of hypertension is clearly increased among the overweight persons, the pathophysiological mechanisms underlying this frequent association of obesity and hypertension are still poorly understood. The expansion of extracellular volume, inducing hypervolaemia and increased cardiac output, represents the characteristic haemodynamic feature of the obesity-related hypertension. The maintenance of hypervolemia in the face of elevated blood pressure, indicates a resetting of pressor natriuresis toward higher blood pressure. The development of hypertension also indicates an increase in peripheral vascular resistance, thus the lack of physiological adaptation of peripheral resistance to increased cardiac output. The mechanisms underlying these changes in renal function and vascular reactivity can no longer be attributed to hyperinsulinaemia as such, but might be related to insulin resistance responsible for the enhancement in pressor activity of noradrenaline and angiotensin II. This increased reactivity to pressor factors may be due to an inadequate nitric oxide generation by vascular endothelium and to increased sodium and calcium concentration in vascular smooth muscle cells. The role of increased neuropeptide Y (NPY) activity, may also be involved. As to enhancement of tubular sodium reabsorption, it could be related to histological changes within the renal medulla, leading to compression of tubules and vasa recta, hence a more efficient sodium reabsorption. As to the therapeutic approach, the low-energy sodium-restricted diet associated with increased physical activity, represents the cornerstones of treatment for the obesity-related hypertension. If this approach fails, the pharmacological treatment becomes necessary, and the use of the converting enzyme inhibitors seems to be the most appropriate choice of drug therapy for hypertensive obese patients.     

Obesity hypertension, salt sensitivity and insulin resistance

AIM: To review human and animal data describing the complex interrelation between obesity hypertension, salt-sensitivity and insulin resistance. DATA SYNTHESIS: The first part of the article reviews the information available in the literature defining obesity hypertension as a salt sensitive form of hypertension and that links obesity hypertension to the presence of insulin. The second part reviews the four factors frequently cited as possible causes for this sodium retention: insulin resistance, alteration in the renin-angiotensin system, altered vascular responsiveness and alterations in the sympathetic nervous system. Special emphasis is given in an attempt to explain how each of these four factors can change pressure-natriuresis. CONCLUSIONS: There is clearly a strong relationship between obesity hypertension, sodium sensitivity and insulin resistance. The exact mechanism responsible for linking these three conditions is still unknown. However, there is ample evidence to suggest that insulin resistance, altered vascular responsiveness, altered function of the renin-angiotensin aldosterone system and altered function of the sympathetic nervous system are important in these three conditions. Further investigation is warranted to completely elucidate the complex relationship between insulin resistance, obesity hypertension and sodium sensitivity.