Purpose of review
Obesity, which has reached epidemic prevalence, is now recognized as an independent risk factor for increasing blood pressure. The complex mechanisms of obesity-related hypertension are unclear, but several studies have provided evidence of a hypertensive shift in pressure natriuresis. Excess sympathetic outflow to the kidneys and changes in renal structure and function may both affect the renal pressure relationship. Other factors that may contribute to altered natriuresis include hyperinsulinemia, hyperleptinemia and activation of the renin-angiotensin system. Disruption of the renal α2 adrenoceptors or leptin
receptor implicated in natriuresis control may also be an additive risk for the increase in tubular reabsorption in obesity hypertension.
Recent advances have highlighted the importance of two adipocyte-derived hormones - leptin
- in obesity hypertension. Leptin
has direct central effects that increase sympathetic outflow to the kidney and the new concept of selective leptin
resistance, suggests the maintenance of leptin
-induced sympathetic activation in obesity, despite resistance to leptin
metabolic effects. On the other hand, a recent study showed that angiotensinogen
produced in the adipocyte is also relevant to blood pressure control.
The article reviews the factors implicated in the disruption of blood pressure control in obesity. Further investigation on the time course of the disease would reveal the relative importance of each of the factors that influence the risk of hypertension in obese individuals.