The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi: 10.1038/hr.2010.9

Kotsis, V., Stabouli, S., Papakatsika, S., Rizos, Z., Parati, G. (2010). Mechanisms of obesity-induced hypertension. HYPERTENSION RESEARCH, 33(5), 386-393 [10.1038/hr.2010.9].

Mechanisms of obesity-induced hypertension

PARATI, GIANFRANCO
2010

Abstract

The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi: 10.1038/hr.2010.9
Articolo in rivista - Articolo scientifico
Leptin; Obesity; Pressure natriuresis; Rennin-angiotensin-aldosterone system; Sympathetic nervous system;
English
2010
33
5
386
393
none
Kotsis, V., Stabouli, S., Papakatsika, S., Rizos, Z., Parati, G. (2010). Mechanisms of obesity-induced hypertension. HYPERTENSION RESEARCH, 33(5), 386-393 [10.1038/hr.2010.9].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/16830
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