Mechanisms of hypertension in obesity.
We conclude that the following may explain the rise in blood pressure with obesity and the subsequent fall in blood pressure (Fig. 2): (1) An increase in calories, protein, or carbohydrate leads to an increase in plasma catecholamines, sympathetic nervous system activity, and insulin secretion. (2) These factors, in turn, lead to increased renal sodium retention and stimulation of the renin-aldosterone system which, in turn, leads to: (3) An increased cardiac output with an inability to appropriately adjust the peripheral resistance to maintain normotension with resultant hypertension. Conversely, the fall in blood pressure with weight reduction can be explained by (Fig. 3): (1) A decrease in calorie, carbohydrate, or protein intake which leads to: (2) A decrease in circulating plasma catecholamines, sympathetic nervous system activity, and insulin secretion which results in: (3) A natriuresis and decrease in the renin-aldosterone system, which causes a decrease in circulating blood volume and in cardiac output. This, in turn, lowers blood pressure towards normal. The unanswered question still remains: why do some obese patients become hypertensive and others remain normotensive? Perhaps there are weight-sensitive individuals and weight-resistant individuals just as there appear to be salt-sensitive and salt-resistant hypertensive patients. Perhaps the answer is genetic. These questions also remain to be answered.
Dornfeld
L P
LP
School of Medicine University of California, Los Angeles 90024.
Maxwell
M H
MH
Waks
A
A
Tuck
M
M
D000311:Adrenal Glands / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D007328:Insulin / Q000502:physiology; D009765:Obesity / Q000150:complications*; D012084:Renin-Angiotensin System; D012964:Sodium / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology
D007328:Insulin; D012964:Sodium