The Effect of Insulin on the Rise in Blood Pressure and Plasma Aldosterone after Angiotensin II in Normal Man

Vierhapper, H; Waldhäusl, W.; Nowotny, Peter

doi:10.1042/cs0640383

Cited by 38 publications

(22 citation statements)

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“…39 In contrast, and once again showing important differences between fructose-or sucrose-fed models, in obese fatfed dogs aldosterone is progressively increased in parallel with sodium accumulation. 8 To explain this inadequate increase, it has been argued that insulin enhances angiotensin-stimulated aldosterone secretion 41 ; however, it is unclear why in the fructose-or sucrose-fed models, which are comparably hyperinsulinemic, aldosterone is not similarly increased.…”

Section: Fructose-feeding and Hypertension Mechanismsmentioning

confidence: 99%

High-fructose feeding elicits insulin resistance, hyperinsulinism, and hypertension in normal mongrel dogs.

1994

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To determine whether chronic high-fructose feeding causes insulin resistance and hypertension in normal dogs, we fed 10 male dogs a normosodic diet containing 60% of the calories as fructose for 20 to 28 days; a control group of 8 dogs was fed a similar diet containing dextrose instead of fructose. In the fructose-fed group, (1) fasting triglyceridemia increased from 35.3±0.63 to 91.9±11.55 mg/dL after 25 days (f <.001); (2) fasting insulinemia increased from 19.0±1.9 to 58.9±7.22 iU/mL after 25 days (P<.001); (3) insulin resistance, which was estimated by steady-state glycemia during an insulin suppression test, increased from 105.8±21.5 to 187.8±32.6 mg/dL after 15 days (/ > <.001), whereas steady-state insulinemia did not change; (4) mean arterial pressure increased from 100.4±1.6 to 122.6±2.3 mm Hg after 28 days (P<.0l); and (5) cumulative sodium balance was increased on days 7 through 11 (111.60±4.44 mEq on day 8, P<.01), returning to T here is overwhelming epidemiologic evidence that insulin resistance and hyperinsulinemia are strongly associated with hypertension. 1 A constellation of cardiovascular risk factors fostered by insulin resistance, including alterations in the circulating lipidic profile (such as hypertrigryceridemia and hypercholesterolemia with high low-density lipoprotein and low high-density lipoprotein cholesterol), atherosclerosis, and hypertension, has been described and conventionally called "syndrome X." 2 The frequent association between non-insulin-dependent diabetes mellitus, obesity, and hypertension has been tentatively ascribed to the presence of insulin resistance. -3 However, a marked impairment in insulin action has also been demonstrated in nonobese, nondiabetic essential hypertensive subjects. 4 Insulin resistance and hypertension have been induced in rodents by chronic high-sucrose or highfructose feeding. 5 These models have provided important information regarding the biochemical mechanisms responsible for the impairment of insulin activity. normal for the rest of the experiment. All these parameters were similar between the fructose-fed and dextrose-fed groups before the diets were started and remained constant in the dextrose-fed group. Neither group showed any change in body weight, fasting plasma glucose, atrial natriuretic factor, or endothelin-1 levels. We conclude that chronic high-fructose feeding elicits hypertriglyceridemia, insulin resistance, hyperinsulinemia, hypertension, and a transient sodium retention in dogs without fostering fasting hyperglycemia or weight gain. Endothelin and atrial natriuretic factor do not appear to play a role in the development of hypertension in this model. However, despite these advances, the pathogenic mechanisms that relate insulin resistance to hypertension remain undefined. Most of our knowledge about the homeostatic mechanisms responsible for coupling the renal excretion of sodium to the control of blood volume and blood pressure has been obtained in dogs 7 ; however, to date there have been no available nonobese, ...

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Section: Fructose-feeding and Hypertension Mechanismsmentioning

confidence: 99%

High-fructose feeding elicits insulin resistance, hyperinsulinism, and hypertension in normal mongrel dogs.

1994

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“…In humans, results regarding the effects of insulin on cardiovascular reactivity are also conflicting. Vierhapper et al 14 reported that intravenous insulin with the euglycemic clamp method did not alter blood pressure responses to Ang II in normal humans. Yamamoto et al 13 reported that intravenous insulin attenuated blood pressure responses to phenylephrine and Ang II in diabetic men without neuropathy.…”

Section: Effect Of Insulin On Vascular Reactivity To Pressor Agentsmentioning

confidence: 99%

“…Most of these studies demonstrated that insulin decreased or did not alter vascular reactivity to vasoconstricting stimuli. 13 ' 14 However, Gans et al 15 recently reported that intravenous insulin augmented blood pressure responses to norepinephrine but not to Ang II. Thus, reported results are conflicting.…”

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confidence: 99%

Intra-arterial infusion of insulin attenuates vasoreactivity in human forearm.

et al. 1993

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Hyperinsulinemia may contribute to the development of hypertension. The aim of the present study was to determine whether hyperinsulinemia modulates vascular reactivity to phenylephrine or angiotensin II. In 10 young, healthy volunteers, the left brachial artery was cannulated for drug infusion and direct measurements of arterial pressure. We measured forearm blood flow by a strain-gauge plethysmograph while infusing phenylephrine (0.2, 0.8, and 2.4 /ig/min) and angiotensin II (5,10, and 20 ng/min) locally into the brachial artery before and during simultaneous intra-arterial infusion of insulin (0.15 mU/kg per minute). Forearm vascular resistance was calculated from directly measured arterial pressure and forearm blood flow. Intra-arterial infusion of insulin raised the local plasma insulin level from 10.3 ±1.4 to 133.3±21.1 /iU/mL (P<.01) and did not change blood glucose level in the venous effluents of the forearm. Insulin infusion slightly but not significantly increased basal forearm blood flow (4.6 ±1.5 to 5.5±0.9 mL/min per 100 milliliters, NS) and decreased forearm vascular resistance (22.1±2.1 to 20.3±2.8 U, NS). Phenylephrine and angiotensin II increased forearm vascular resistance dose dependently before and during simultaneous insulin infusion (P<.01 for both). Intra-arterial infusion of insulin attenuated vascular reactivity to phenylephrine (P<.01) and angiotensin II (P<.01). None of these drugs changed blood pressure or heart rate. Our results suggest that hyperinsulinemia attenuates vascular reactivity in the forearm resistance vessels in healthy humans.

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“…However, there are limited data on the microvascular effects of insulin in man. Euglycaemic hyperinsulinaemia in healthy subjects has been reported to augment cardiovascular reactivity to noradrenaline [19], while no effect was demonstrated with angiotensin II [19,20]. Moreover, acute increases in plasma insulin within the physiological range have shown conflicting responses in forearm vasodilation [21,22], but with no increase in blood pressure despite increased sympathetic neural outflow [21] and a marked increase in forearm noradrenaline release [22].…”

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confidence: 99%

The effect of insulin on the vascular reactivity of isolated resistance arteries taken from healthy volunteers

et al. 1995

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Summary Impaired reactivity of the resistance vasculature may contribute to the development of diabetic microangiopathy by altering microvascular haemodynamics. This study investigates the acute effects of insulin on the contractility and relaxation properties of isolated human resistance arteries (< 300 ~tm internal diameter) taken from gluteal subcutaneous fat of 33 (18 male: 15 female) normotensive healthy volunteers (supine blood pressure 115.6 + 1.6/ 70.0 + 1.5 mmHg [mean + SEM], with no family history of hypertension or diabetes mellitus. Resistance arteries were mounted in a small vessel myograph to measure isometric tension. Contractile responses to noradrenaline were reduced after incubation in 1 mU/ml of insulin for 20 min (p < 0.01; Group 1). Increasing concentrations of insulin were found to reduce the contractile response to noradrenaline in a dose-dependent manner (Group2; 0.1mU/ml by 8% [p

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The Effect of Insulin on the Rise in Blood Pressure and Plasma Aldosterone after Angiotensin II in Normal Man

Cited by 38 publications

References 0 publications

High-fructose feeding elicits insulin resistance, hyperinsulinism, and hypertension in normal mongrel dogs.

High-fructose feeding elicits insulin resistance, hyperinsulinism, and hypertension in normal mongrel dogs.

Intra-arterial infusion of insulin attenuates vasoreactivity in human forearm.

The effect of insulin on the vascular reactivity of isolated resistance arteries taken from healthy volunteers

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