Obesity-induced hypertension: Renal function and systemic hemodynamics

This study examined the control of renal hemodynamics and tubular function, as well as systemic hemodynamics, during obesity-induced hypertension in chronically instrumented conscious dogs. Mean arterial pressure, cardiac output, and heart rate were monitored 24 hours a day using computerized methods, water and electrolyte balances were measured daily, and renal hemodynamics were measured each week during the control period and 5 weeks of a high-fat diet. After 7 to 10 days of control measurements, 0.5 to 0.9 kg of cooked beef fat was added to the regular diet, and sodium intake was maintained constant at 76 mmol/d throughout the study. After 5 weeks of the high-fat diet, body weight increased from 24.0±1.0 to 35.9±4.9 kg, mean arterial pressure increased from 83±5 to 100±4 mm Hg, cardiac output increased from 2.86±0.27 to 4.45±0.55 L/min, and heart rate rose from 68±5 to 107±9 beats per minute. Associated with the hypertension was an increase in cumulative sodium balance to 507±107 mmol after 35 days and a rise in sodium iothalamate space, an index of extracellular fluid volume, to 131±4% of control. Sodium retention was due to increased tubular reabsorption, because glomerular filtration rate and effective renal plasma flow increased throughout the 5 weeks of the high-fat diet, averaging 135±4% and 149±19% of control, respectively, during the fifth week of the high-fat diet Plasma renin activity and plasma insulin concentration increased from 0.46±0.12 ng angiotensin I/mL per hour and 11.1±2.6 μU/mL, respectively, to 1.10±0.23 ng angiotensin I/mL per hour and 30.1±7.0 μU/mL after 5 weeks. Because decreased sodium excretion occurred despite elevated mean arterial pressure, obesity-induced hypertension in dogs is associated with a shift of renal pressure natriuresis that is caused by increased tubular reabsorption, although the exact mechanism by which this occurs is still unclear.