Obesity-hypertension: The effects on cardiovascular and renal systems

Longitudinal and cross-sectional studies suggest that a large number of obe se patients have a high prevalence of hypertension. This association causes the following changes: insulin and leptin resistance with a suppressed bio logic activity of natriuretic peptide, which contributes to sodium retentio n with concomitant expanded cardiopulmonary volume and increased cardiac ou tput. The cellular metabolism of cations may be altered in obesity and may lead to changes in vascular responsiveness and increased vascular resistanc e. These changes lead to structural adaptations in the heart characterized by concentric-eccentric left ventricular hypertrophy. The hypertrophic cond ition provides the basis for the development of congestive heart failure an d cardiac arrhythmias that may explain the higher rates of cardiac sudden d eath in those patients. In the kidneys, obesity hypertension may initiate a derangement of renal function. The increased deposit of interstitial cells and of extracellular matrix between the tubules induces higher interstitia l hydrostatic pressure and tubular sodium reabsorption. The consequent incr ease in renal now and glomerular filtration enhances albuminuria excretion and the susceptibility to the development of renal damage. In summary, the hemodynamic and structural adaptations related to obesity hypertension is t he cause of greater risk for adverse cardiovascular and renal events. Am J Hypertens 2000;13:1308-1314 (C) 2000 American Journal of Hypertension, Ltd.