Obesity-associated hypertension: hypothesized link between etiology and selection of therapy

The association of obesity and hypertension is characterized hemodynamically by an increase in absolute circulating intravascular volume that induces increased cardiac output and total peripheral resistance that remains inappropriately normal. These changes constitute the hemodynamic basis for the increase in blood pressure in obesity. Obesity-associated hypertension is also characterized by an abnormal renal response, including increased renal blood flow and a rise in glomerular and interstitial pressures. These hemodynamic changes induce the following structural changes in the heart: enlarged left atrial, ventricular and aortic root diameters as well as increased posterior septal wall thickness and left ventricular mass. The hemodynamic changes in the kidneys generate higher glomerular volume and increased interstitial infiltrate, which may cause compression of the tubules and blood vessels of the renal medulla. Weight reduction is an effective tool in the control of blood pressure, and significantly reduces the metabolic and hemodynamic derangements that occur with obesity. However, since weight reduction compliance is difficult to maintain, pharmacological agents are often needed to control blood pressure. Angiotensin-converting enzyme inhibitors, calcium channel blockers and alpha- adrenergic blocking agents may be the most appropriate therapy for obesity-associated hypertension since they intervene with some of the previously described pathophysiological conditions.