Obese subjects often have
hypertension and related cardiovascular and renal diseases, and this has become a serious worldwide health problem. In obese subjects, impaired renal-pressure natriuresis causes
sodium retention, leading to the development of
salt-sensitive
hypertension. Physical compression of the kidneys by visceral fat and activation of the sympathetic nervous system,
renin-
angiotensin systems (RAS), and
aldosterone/
mineralocorticoid receptor (MR) system are involved in this mechanism. Obese subjects often exhibit
hyperaldosteronism, with increased
salt sensitivity of blood pressure (BP). Adipose tissue excretes
aldosterone-releasing factors, thereby stimulating
aldosterone secretion independently of the systemic RAS, and
aldosterone/MR activation plays a key role in the development of
hypertension and organ damage in
obesity. In obese subjects, both
salt sensitivity of BP, enhanced by
obesity-related metabolic disorders including
aldosterone excess, and increased
dietary sodium intake are closely related to the incidence of
hypertension. Some
salt sensitivity-related gene variants affect the risk of
obesity, and together with
salt intake, its combination is possibly associated with the development of
hypertension in obese subjects. With high
salt levels common in modern diets,
salt restriction and weight control are undoubtedly important. However, not only MR blockade but also new diagnostic modalities and
therapies targeting and modifying genes that are related to
salt sensitivity,
obesity, or RAS regulation are expected to prevent
obesity and
obesity-related
hypertension.