Pathophysiology and treatment of the obesity-related arterial hypertension.

J Kolanowski
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引用次数: 5

Abstract

While obesity is frequently associated with arterial hypertension, the underlying mechanism is still poorly understood. A marked drop in blood pressure in response to hypocaloric carbohydrate-poor diet, occurring usually in obese hypertensive patients even before any significant reduction of body weight is achieved, strongly suggests that the obesity related metabolic abnormalities rather than the degree of fatness as such, are involved in the association between obesity and overweight. Among several possible mechanisms, the state of insulin resistance with hyperinsulinaemia, as well as increased activity of the sympathetic nervous system, are probably responsible for the development of arterial hypertension in obese subjects. The arterial hypertension may be promoted by these two mechanisms, which are probably causally related, closing the pathophysiologic loop leading to hypertension. Both mechanisms may promote the development of haemodynamic abnormalities which characterize the hypertension associated with obesity, i.e. the renal sodium and fluid retention with ensuing expansion of the extracellular volume and the increased peripheral vascular resistance.

肥胖相关性高血压的病理生理及治疗。
虽然肥胖经常与动脉高血压相关,但其潜在机制仍然知之甚少。低热量低碳水化合物饮食导致的血压明显下降,通常发生在肥胖高血压患者,甚至在体重显著减轻之前,这强烈表明肥胖相关的代谢异常,而不是肥胖程度本身,与肥胖和超重之间的关系有关。在几种可能的机制中,高胰岛素血症的胰岛素抵抗状态以及交感神经系统活动的增加可能是肥胖受试者动脉高血压发生的原因。这两种机制可能促进了动脉性高血压的发生,它们之间可能存在因果关系,关闭了导致高血压的病理生理回路。这两种机制都可能促进血液动力学异常的发展,这是肥胖相关高血压的特征,即肾钠和液体潴留,随之而来的是细胞外体积的扩大和周围血管阻力的增加。
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