TY - JOUR
T1 - Mechanisms in obesity-related hypertension
T2 - Role of insulin and catecholamines
AU - Krieger, Diane R.
AU - Landsberg, Lewis
N1 - Funding Information:
From the Dana-Thorndike Laboratories, Department of Medicine, Beth Israel Hospital, and Harvard Medical School. This work was supported in part by USPHS grants DK20378, HL37871, HL36568, and AG00599. Address correspondence and reprint requests to Dr Landsberg, Department of Medicine, Beth Israel Hospital, Boston, MA 02215.
PY - 1988/1
Y1 - 1988/1
N2 - Although the association of obesity and hypertension is well recognized, the mechanisms involved in the pathogenesis of increased blood pressure in the obese are poorly understood. Recent studies addressing the impact of 1) body fat distribution on blood pressure and 2) dietary intake on sympathetic nervous system (SNS) activity suggest a plausible hypothesis that relates the hypertension of the obese to hyperinsulinemia and SNS stimulation. Hypertension in the obese is associated with fat accumulation in the upper body segments; this type of obesity is also characterized by hyperinsulinemia and insulin resistance. Insulin, moreover, is an important signal in the relationship between dietary intake and SNS activity: increased insulin levels are associated with SNS stimulation. The hyperinsulinemia of obesity may, therefore, increase blood pressure by 1) direct effects of insulin to stimulate renal sodium reabsorption, and 2) sympathetic stimulation of the heart, blood vessels, and kidney. Conversely, SNS suppression and diminished insulin following caloric restriction may explain the hypotensive effects of caloric restriction in obese hypertensive subjects. The hypothesis presented here emphasizes the important role of diet in the treatment of obese hypertensive subjects. The efficacy of caloric restriction, weight loss, and exercise in reducing blood pressure in the obese is linked to diminished insulin and SNS activity and may be viewed as evidence in favor of this hypothesis. Am J Hypertens 1:84-90, 1988.
AB - Although the association of obesity and hypertension is well recognized, the mechanisms involved in the pathogenesis of increased blood pressure in the obese are poorly understood. Recent studies addressing the impact of 1) body fat distribution on blood pressure and 2) dietary intake on sympathetic nervous system (SNS) activity suggest a plausible hypothesis that relates the hypertension of the obese to hyperinsulinemia and SNS stimulation. Hypertension in the obese is associated with fat accumulation in the upper body segments; this type of obesity is also characterized by hyperinsulinemia and insulin resistance. Insulin, moreover, is an important signal in the relationship between dietary intake and SNS activity: increased insulin levels are associated with SNS stimulation. The hyperinsulinemia of obesity may, therefore, increase blood pressure by 1) direct effects of insulin to stimulate renal sodium reabsorption, and 2) sympathetic stimulation of the heart, blood vessels, and kidney. Conversely, SNS suppression and diminished insulin following caloric restriction may explain the hypotensive effects of caloric restriction in obese hypertensive subjects. The hypothesis presented here emphasizes the important role of diet in the treatment of obese hypertensive subjects. The efficacy of caloric restriction, weight loss, and exercise in reducing blood pressure in the obese is linked to diminished insulin and SNS activity and may be viewed as evidence in favor of this hypothesis. Am J Hypertens 1:84-90, 1988.
KW - Catecholamines
KW - Hyperinsulinemia
KW - Insulin
KW - Neuroendocrine mechanisms
KW - Obesity-related hypertension
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U2 - 10.1093/ajh/1.1.84
DO - 10.1093/ajh/1.1.84
M3 - Article
C2 - 3285861
AN - SCOPUS:0023939656
SN - 0895-7061
VL - 1
SP - 84
EP - 90
JO - American Journal of Hypertension
JF - American Journal of Hypertension
IS - 1
ER -