Does Chronic Hyperinsulinemia Cause Hypertension?

Je, Hall; Tg, Coleman; Hl, Mizelle

doi:10.1093/ajh/2.3.171

Cited by 53 publications

(21 citation statements)

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“…Chronic experimental hyperinsulinemia in normal dogs did, however, not produce hypertension (27), not even if their kidney mass was reduced and they were given a high sodium loaded diet. Moreover, patients with high insulin levels caused by insulinoma did not become hypertensive, and their blood pressure did not change after operation leading to normalised s-insulin concentration (28) .…”

Section: Discussionmentioning

confidence: 94%

The Interrelationships between Fasting Serum Insulin Level, Obesity and Blood Pressure in Women: Results from a Cross-Sectional Population Study of Women in Gothenburg, Sweden.

Kristjansson¹,

Lissner

Bengtsson³

et al. 1993

Hypertens Res

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This study is based on a representative population sample of women in Gothenburg, Sweden. Three hundred and thirty-six 50-year-old nondiabetic women, not taking any antihypertensive medication, were included in the study. They underwent a comprehensive examination programme, where body weight, body height, waist and hip circumferences, systolic and diastolic blood pressures and fasting serum insulin concentration were measured. Fasting serum insulin concentration was significantly correlated with systolic and diastolic blood pressures. After controlling for both body mass index (BMI) and waist to hip circumference ratio (WHR), fasting serum insulin concentration remained independently associated with blood pressure (P = 0.001 for systolic blood pressure, P = 0.06 for diastolic blood pressure). When stratified for BMI or WHR the correlations between fasting serum insulin concentration and blood pressure remained significant only in the upper 50th precentiles of BMI and WHR. When relating pressure to different levels of fasting serum insulin concentration there seems to be a threshold at an insulin concentration corresponding to the upper quartile limit (at approximately 17 uU/ml), above which level the blood pressure rises more obviously. The same phenomenon was seen for systolic and diastolic blood pressures. (Hypertens Res 1993; 16: 197-201)

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Section: Discussionmentioning

confidence: 94%

The Interrelationships between Fasting Serum Insulin Level, Obesity and Blood Pressure in Women: Results from a Cross-Sectional Population Study of Women in Gothenburg, Sweden.

Kristjansson¹,

Lissner

Bengtsson³

et al. 1993

Hypertens Res

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“…At time 0, glucose (300 mg/kg) was injected in 1 minute. Additional samples were collected at 2,3,4,5,6,8,10,12,14,16,19,22,25,30,40,50,60,70,80,90,100,110,120,140,160,180,210, and 240 minutes. Blood was rapidly centrifuged and glucose immediately measured by the glucose oxidase method with an automated glucose analyzer (Beckman Instruments Inc., Fullerton, Calif.).…”

Section: Frequently Sampled Intravenous Glucose Tolerance Testmentioning

confidence: 99%

“…Although several studies give evidence of high peripheral insulin levels in hypertension, 5 -6 - 8 there are only a few investigations on dynamic beta cell function and insulin resistance in this state. 6 To our knowledge, the role of hepatic insulin extraction in the pathogen-esis of hyperinsulinemia in essential hypertension has not been elucidated so far.…”

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confidence: 99%

Elevated hepatic insulin extraction in essential hypertension.

et al. 1993

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Insulin resistance, hyperinsulinemia, and dyslipidemia are common characteristics of patients with untreated hypertension. However, the link between the vascular and metabolic disturbances is still unclear. To provide further insights into the metabolic picture of subjects with hypertension, we evaluated insulin resistance, pancreatic secretion, and hepatic extraction of the hormone in 16 untreated patients with essential hypertension before and after 12-16 weeks of drug treatment in comparison with 16 age-, sex-, and body weight-matched normotensive control subjects. All subjects underwent an oral and a frequently sampled intravenous glucose tolerance test. Metabolic parameters were calculated by the minimal model technique. The hypertensive patients exhibited a highly reduced tissue insulin sensitivity (2.6±0.4 versus 9.6±1.9 10 4 min~V[microunits/mL];p<0.001). The basal secretion rate (70+11 versus 35±5 pmol/L per minute) and the total amount of prehepatically secreted insulin (32±4 versus 16±2 nmol/L in 4 hours) were significantly increased in the hypertensive patients compared with the control subjects (p<0.01), whereas the posthepatic insulin delivery rate was not significantly different between the two groups (4.9±0.6 versus 3.5 ±0.3 nmol/L in 4 hours). Hepatic insulin extraction was found to be significantly elevated in the hypertensive patients compared with control subjects (81±4% versus 69±3%, p<0.04). Increased hepatic insulin extraction partially ameliorated B cell hypersecretion in hypertensive patients. After 12-16 weeks of drug treatment, the blood pressure was normalized, but the metabolic profile of the patients remained unchanged. We conclude that elevated insulin extraction in the liver is a specific characteristic of individuals with essential hypertension and partially compensates pancreatic B cell hypersecretion. {Hypertension 1993;21:646-653) KEY WORDS • hypertension, essential • insulin sensitivity • hepatic insulin extraction T he striking clinical association among hypertension, hyperinsulinemia, and impaired glucose tolerance has attracted considerable attention in recent years, 1 " 3 but despite great scientific effort the etiology and pathogenesis of these diseases and the link between high blood pressure and the metabolic aberrations are still unknown.4 -8 Because these conditions represent predictors for cardiovascular disease and early mortality, it would be of great interest to elucidate the hyperinsulinemia-hypertension link. Moreover, it is still controversial whether drug treatment leads to changes in the metabolic status of patients with essential hypertension and has any effect on coronary artery disease at all.Although several studies give evidence of high peripheral insulin levels in hypertension, 5 -6 -8 there are only a few investigations on dynamic beta cell function and insulin resistance in this state. 6 To our knowledge, the role of hepatic insulin extraction in the pathogen- esis of hyperinsulinemia in essential hypertension has not been elucidated so far. Therefor...

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“…20 Also, obese hypertensive patients have concomitant hyperinsulinemia and increased plasma glucose. Hyperinsulinemia has been postulated to increase blood pressure in obese hypertensive patients.…”

Section: Figure 4 Bar Graph Showing Effect Of Insulin Infusion (10 mentioning

confidence: 99%

Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

et al. 1990

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Although hyperinsulinemia and increased adrenergic activity have been postulated to be important factors in obesity-associated hypertension, a cause and effect relation between insulin, catecholamines, and hypertension has not been established. The aim of this study was to determine whether chronic hyperinsulinemia, comparable with that found in obese hypertensive patients, causes hypertension in normal dogs, increases plasma catecholamines, or potentiates the blood pressure effects of norepinephrine. In six normal dogs, insulin infusion (1.0 milliunits/ kg/min) for 7 days, with euglycemia maintained, increased fasting insulin fourfold to sixfold. However, mean arterial pressure did not increase, averaging 99 ±2 mm Hg during the control period and 91 ±3 mm Hg during the 7 days of insulin infusion. Insulin did not alter plasma norepinephrine or epinephrine, which averaged 171±27 and 71±14 pg/ml, respectively, during the control period and 188 ±29 and 45 ±12 pg/ml during the 7 days of insulin infusion. In six dogs, norepinephrine was infused (0.2 /tig/kg/min) for 7 days to raise plasma norepinephrine to 2,940±103 pg/ml. Insulin infusion (1.0 milliunits/kg/min) for 7 days during simultaneous infusion of norepinephrine did not further increase mean arterial pressure, which averaged 101 ±3 during norepinephrine and 98 ±2 mm Hg during insulin plus norepinephrine infusion. Thus, chronic hyperinsulinemia did not increase mean arterial pressure or plasma catecholamines and did not potentiate the blood pressure actions of norepinephrine. These observations provide no evidence that chronic hyperinsulinemia or interactions between insulin and plasma catecholamines cause hypertension in normal dogs. (Hypertension 1990;15:519-527) A association between obesity and hypertension has been noted by numerous investigators, and reductions in caloric intake and body weight often lower blood pressure in obese hypertensive patients.1 -3 Several lines of indirect evidence suggest that insulin could be an important link between changes in caloric intake, activity of the sympathetic nervous system, and hypertension associated with obesity. 4 -5 Increased caloric intake because of carbohydrate ingestion elevates insulin levels and appears to activate the sympathetic nervous system, whereas caloric restriction suppresses insulin and sympathetic activity as assessed by variFrom the

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Does Chronic Hyperinsulinemia Cause Hypertension?

Cited by 53 publications

References 0 publications

The Interrelationships between Fasting Serum Insulin Level, Obesity and Blood Pressure in Women: Results from a Cross-Sectional Population Study of Women in Gothenburg, Sweden.

The Interrelationships between Fasting Serum Insulin Level, Obesity and Blood Pressure in Women: Results from a Cross-Sectional Population Study of Women in Gothenburg, Sweden.

Elevated hepatic insulin extraction in essential hypertension.

Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

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