Obesity prevalence factors associated with sympathetic overactivity and hypertension

Abstract

BackgroundObesity is the most significant worldwide public health problem and is integrally related to negative cardiovascular disease and hypertension results. The association between obesity and overweight elevated blood pressure is well known, and so it is calculated that 65%–78% of primary hypertension cases are accounted for by obesity.AimThis study aims to focus on whether obesity prevalence factors are associated with sympathetic overactivity and hypertension.MethodsThe pathways by which hypertension is induced by obesity are complicated and involve overactivation of the sympathetic nervous system (SNS), enhancement of the renin‐angiotensin‐aldosterone system (RAAS), modifications in cytokines produced from adipose, tolerance to insulin, and structural and functional renal changes.ResultsObesity induces the activation of mineralocorticoid receptors independently of aldosterone or angiotensin II (ANG II). The SNS activation mechanism in obesity has not been completely elucidated; however, leptin and activation of the melanocortin brain system may be needed. Obesity‐associated hypertension becomes much more challenging to handle with continuous obesity, and the progression of target organ injury, especially renal injury, multiple antihypertensive medications, and other medical conditions, such as dyslipidemia, insulin resistance, diabetes mellitus, and inflammation, are also needed.ConclusionThis review aimed to address the consequences of obesity and SNS function, risk factors, the impact of obesity, pharmacological treatment strategies for managing, and recommended exercise and diet.

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