Abstract
Obesity-associated hypertension is a serious public health concern. Sympathetic nervous system (SNS) overactivity, especially in the kidneys, is an important mechanism linking obesity to hypertension. Some adipokines play important roles in elevating blood pressure (BP). Hyperinsulinemia caused by insulin resistance stimulates sodium reabsorption, enhances sodium retention, and increases circulating plasma volume. Hyperinsulinemia also stimulates both the renin-angiotensin-aldosterone system (RAAS) and the SNS, resulting in the acceleration of atherosclerosis through the hypertrophy of vascular smooth muscle cells, which contributes to increased peripheral vascular resistance. Obesity is associated with increased RAAS activity despite volume overload, as the tissue RAASs are stimulated in obese hypertensive individuals. Mineralocorticoid receptor-associated hypertension must also be considered in obese patients with resistant hypertension. Obstructive sleep apnea syndrome (OSAS) is the most common cause of secondary hypertension. Some components of the gut microbiota contribute to BP control; therefore, gut dysbiosis caused by obesity might lead to increased BP. The ratio of visceral fat to subcutaneous fat is higher in Japanese patients than in Caucasian patients, which may explain why Japanese patients are more susceptible to metabolic disorders even though they are less obese than Caucasian individuals. Obesity-associated kidney dysfunction directly increases BP, leading to further deterioration of kidney function. A bodyweight reduction of more than 3% or 5 kg significantly lowers BP. Gastrointestinal bypass surgery is an effective treatment for morbid obesity and its related metabolic disorders, including hypertension. Because both obesity and hypertension are representative lifestyle-related disorders, lifestyle modification, especially to improve obesity, should be performed first as a treatment for hypertension.
