From big fat cells to high blood pressure: a pathway to obesity-associated hypertension

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Purpose of review

The environment created by modern industrialized societies has caused an unprecedented rise in the prevalence of obesity and obesity-related disorders, including hypertension. Mechanisms that underlie the development of hypertension in obese individuals are not very well understood; they are thought to involve activation of the sympathetic nervous system, the renin–angiotensin–aldosterone system, and oxidative stress.

Recent findings

Recent research suggests that obesity-associated hypertension may be causally related to the accumulation of ‘dysfunctional’ adipose tissue characterized by the presence of ‘large’ lipid-laden adipocytes.


Excess energy-intake leads to an expansion of adipose tissue, a hallmark of obesity. But morphology of the expanded adipose tissue differs across individuals, including the size of adipocytes. The presence of ‘large’ rather than ‘small’ adipocytes is associated with functional and structural abnormalities of adipose tissue. These include increased production of bioactive molecules, such as leptin, angiotensinogen, pro-inflammatory cytokines, and reactive oxygen species; insufficient capacity to accommodate excess energy-intake leading to ectopic fat storage in tissues and in turn insulin resistance and hyperinsulinemia; and augmented macrophage infiltration enhancing the production of pro-inflammatory cytokines and reactive oxygen species. Such a ‘dysfunctional’ adipose tissue may, in turn, induce activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system and oxidative stress and, hence, promote the development of obesity-associated hypertension.

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