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Despite considerable progress in understanding the pathophysiology of obesity, there are still no specific guidelines for the treatment of obesity hypertension other than weight reduction. Special considerations for obese hypertensive patients, in addition to controlling blood pressure, are correcting the metabolic abnormalities and protecting the kidneys from injury. This remains an important area for further research, especially in view of the current 'epidemic' of obesity in most industrialized countries.

Abstract-This study examined the importance of aldosterone (ALDO) in mediating changes in renal function and increased mean arterial pressure (MAP) during the development of dietary-induced obesity in chronically instrumented dogs. Mean arterial pressure, heart rate (HR), and cardiac output (CO) were recorded 24 hours per day in lean dogs (nϭ7) before and after administration of an ALDO antagonist, eplerenone (EP) (10 mg/kg twice daily), for 10 days. After 10 days of EP treatment, the dogs (nϭ7) were given a supplement of cooked beef fat for 5 weeks while EP was continued. An untreated group (nϭ6) was fed a high fat diet for 5 weeks and used as control (C). In lean dogs, EP decreased MAP from 89Ϯ4 to 84Ϯ4 mm Hg and glomerular filtration rate from 67.4Ϯ6.8 to 53.2Ϯ4.9 mL/min while inducing a small negative Na ϩ balance (Ϫ42Ϯ12 mEq). Plasma renin activity increased from 0.4Ϯ0.1 to 2.7Ϯ0.7 ng AI/mL per hour and plasma K ϩ increased from 4.8Ϯ0.1 to 6.1Ϯ0.3 mEq/L. After 5 weeks of a high fat diet, body weight increased 45% to 53% in EP and C obese dogs. In C dogs, MAP increased by 16Ϯ3 mm Hg, compared with only 7Ϯ1 mm Hg in EPLE dogs. Compared with untreated dogs, the EP dogs had smaller increases in CO (18Ϯ4.6% versus 43Ϯ1.5%), HR (33Ϯ5% versus 60Ϯ3%), glomerular filtration rate (19Ϯ5% versus 38Ϯ6%), and cumulative Na ϩ balance (138Ϯ35 mEq versus 472Ϯ110 mEq) after 5 weeks of a high fat diet. Thus, EP markedly attenuated glomerular hyperfiltration, sodium retention, and hypertension associated with chronic dietary-induced obesity. These observations indicate that ALDO plays an important role in the pathogenesis of obesity hypertension. Key Words: blood pressure Ⅲ renin-angiotensin system Ⅲ kidney Ⅲ sodium Ⅲ potassium Ⅲ glomerular filtration rate Ⅲ cardiac output Ⅲ obesity T he importance of obesity as a cause of hypertension is widely recognized, with experimental studies showing that excess weight gain raises blood pressure, clinical studies demonstrating that weight loss lowers blood pressure in most hypertensive patients, and population studies showing that overweight and obesity are major risk factors for development of hypertension. 1-5 Also, most patients with hypertension are overweight, and evidence from epidemiological studies suggests that 65% to 75% of the risk for human essential hypertension can be directly attributed to excess weight. 4,5 Although the importance of obesity as a cause of hypertension is well established, the mechanisms that link excessive weight gain with increased blood pressure are not as well understood. Previous studies suggest that obesity impairs renal-pressure natriuresis as the result of increased tubular sodium reabsorption. [5][6][7][8] These abnormalities of renal function may be due in part to activation of the renin-angiotensin-aldosterone system (RAAS).Studies in experimental animals and humans have shown that obesity activates most components of the RAAS. 9,10 A significant role for angiotensin II (Ang II) in stimulating renal sodium reabsorption and in contributing to ob...

Drug associations in individuals with CKD were related to high prevalence of serious DIs, especially in the later stages of the disease.