Pathophysiology and treatment of the obesity-related arterial hypertension.
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.
Kolanowski
J
J
Dept. of Physiology, University of Louvain Medical School (UCL), Brussels, Belgium.
D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure; D004038:Diet, Reducing; D005947:Glucose / Q000378:metabolism; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D007333:Insulin Resistance / Q000502:physiology; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D012964:Sodium / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology
D000959:Antihypertensive Agents; D012964:Sodium; D005947:Glucose