Abstract

Arterial hypertension, obesity, the renin-angiotensinaldosterone system (RAAS), and uric acid are all independently ligated to an increased cardiovascular (CV) risk. Arterial hypertension and obesity are among the 20 leading risk factors that increase the mortality of the general population with hypertension, which is number one. In turn, obesity is one of the most common factors responsible for the development of arterial hypertension. On the other hand, the RAAS and uric acid have been shown to participate independently in the development and maintenance of arterial hypertension, as well as in the mechanisms leading to the development of hypertension in obesity. Furthermore, RAAS as well as uric acid have been shown to be related to an increase in CV morbidity and mortality in hypertension and obesity. In fact, uric acid could play a role in the epidemic of obesity-related metabolic syndrome and cardiorenal disease. In this issue of The Journal of Clinical Hypertension, Zhang and colleagues expand the knowledge of the participation of the RAAS and uric acid in the pathogenesis of hypertension in obesity. The authors describe that serum uric acid is strongly related to angiotensinogen in an obesity-dependent manner in untreated hypertensive patients. They also describe that serum uric acid seems to contribute to the enhancement of plasma angiotensinogen and could be involved in the pathophysiology of obesity-related hypertension where an increase in activity of RAAS is one of the mechanisms underlying the development and maintenance of arterial hypertension. The pathophysiological scene of hypertension in obesity is a vicious circle in which specific mechanisms can contribute at the same time to trigger others, leading to the progressive deterioration of the cardiorenal system. This crosstalk between hypertension and obesity is represented in the Figure where it is shown how these mechanisms are interconnected. In this context, hyperuricemia is strongly related to arterial hypertension. At the same time, increased sympathetic activity and increased RAAS are also mechanisms underlying hypertension and obesity, where the results of Zhang and colleagues also point to angiotensinogen as an important player in the pathogenesis of obesity hypertension. The high level of circulating angiotensinogen observed in untreated hypertensive obese patients is also likely

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