Hypertension and Obesity

Abstract

Obesity is a common problem in much of the western world today in that is linked directly with several disease processes, notably, hypertension. It is becoming clear that the adipocyte is not merely an inert organ for storage of energy but that it also secretes a host of factors that interact with each other and may result in elevated blood pressure. Of particular importance is the putative role of leptin in the causation of hypertension via an activation of the sympathetic nervous system and a direct effect on the kidneys, resulting in increased sodium reabsorption leading to hypertension. Obesity per se may have structural effects on the kidneys that may perpetuate hypertension, leading to an increased incidence of end-stage renal disease that results in further hypertension. Adipose tissue may elaborate angiotensin from its own local renin-angiotensin system. The distribution of body fat is considered important in the genesis of the obesity-hypertension syndrome, with a predominantly central distribution being particularly ominous. Weight loss is the cornerstone in the management of the obesity-hypertension syndrome. It may be achieved with diet, exercise, medications, and a combination of these measures. Anti-obesity medications that are currently undergoing clinical trials may play a promising role in the management of obesity and may also result in lowering of blood pressure. Antihypertensives are considered important components in the holistic approach to the management of this complex problem.

Knockdown of angiotensinogen by shRNA-mediated RNA interference inhibits human visceral preadipocytes differentiation

“…1 Obesity and specifically the deleterious form, visceral adiposity, is a fast-growing serious health problem that causes a considerable variety of obesity-related diseases, such as hypertension, cardiovascular diseases and diabetes mellitus. [2][3][4][5] It is known that the underlying cause of obesity is the massive accumulation of subcutaneous and visceral fat as a result of the continuous proliferation and differentiation of preadipocytes. Therefore, molecular identification of adipogenesis during preadipocytes differentiation may strongly promote the understanding of obesity and obesity-associated diseases.…”

Is the prevalence of arterial hypertension in rheumatoid arthritis and osteoarthritis associated with disease?

“…The prevalence of HT is associated with age [27] and BMI [28], which explains the higher prevalence of HT in OA. When the results were adjusted for age and BMI the HT prevalence in RA and OA was similar.…”

“…Upon comparing the rates of newly discovered, treated with antihypertensive therapy and uncontrolled HT in our study with rates in the general Croatian population [29] and rates described for RA [28], there was a lower rate for newly discovered HT (reference 29: 44.5%; reference 28: 39.4% vs. this study: 29.9% and 18.6% for RA and OA, respectively), a higher rate for treated HT (reference 29: 44.5%; reference 28: 60.6% vs. this study: 75.1% and 86.0% for RA and OA, respectively) and a lower rate for uncontrolled HT (reference 29: 85.6%; reference 28: 78.36% vs.…”

Programming of obesity and cardiovascular disease

“…The new concept of leptin resistance suggests the maintenance of leptin-induced sympathetic activation in obesity, despite resistance to leptin metabolic effects. 74 There are several other ways of programming hypertension in early life than by programming excessive adipose tissue development. The maternal nutritional status appeared to programme expression of the renal angiotensin II type 2 receptor.…”