Effect of mild hyperisulinemia on conduit vessel endothelial function

Morgantini, Cecilia; Stea, Francesco; Boldrini, Beatrice; Duranti, Emiliano; Ghiadoni, Lorenzo; Natali, Andrea

doi:10.1097/hjh.0b013e32834f9882

Cited by 10 publications

(6 citation statements)

References 33 publications

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“…The augmented responses to nitroglycerine documented in the present cohort may reflect less neurogenic constraint on the dilator capacity of vascular smooth muscle as a result of diminished MSNA. Indeed, in a recent experiment involving 10 healthy male volunteers submitted to a sympathoexcitatory stimulus, the brachial dilator response to nitroglycerine was augmented by intravenous infusion of the centrally acting sympatholytic drug, clonidine 35. As baseline diameter was not increased, an inhibitory effect of simvastatin on vascular Rho kinase activity36 is less likely.…”

Section: Discussionmentioning

confidence: 99%

Simvastatin reduces sympathetic outflow and augments endothelium-independent dilation in non-hyperlipidaemic primary hypertension

McGowan

Murai

Millar

et al. 2012

Heart

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Section: Discussionmentioning

confidence: 99%

Simvastatin reduces sympathetic outflow and augments endothelium-independent dilation in non-hyperlipidaemic primary hypertension

McGowan

Murai

Millar

et al. 2012

Heart

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“…The lack of homogenous response is also apparent in studies utilizing low dose insulin. Increased limb blood flow was observed in response to insulin infusion rates 0.06-0.5 mU/kg/min [43, 69,97], whereas other studies reported no effects at similar infusion rates [120,135,191]. Furthermore, blood flow reductions have been observed in response to low (0.2 mU/kg/min) or moderate (0.9 mU/kg/min) hyperinsulinemia [8].…”

Section: Effects In Lean Healthy Individualsmentioning

confidence: 99%

“…Yet, studies that use experimental hyperinsulinemia to examine the vascular actions of insulin have shown inconsistent findings. Some of these studies reported enhanced limb blood flow in response to insulin stimulation [40,58,69,171], whereas others demonstrated either null effects or reduction in blood flow [8,80,120,191]. As a result, the prevailing concept that hyperinsulinemia induces vasodilation and improves blood flow may need to be reconsidered.…”

Section: Introductionmentioning

confidence: 99%

Skeletal Muscle Vascular Function: A Counterbalance of Insulin Action

et al. 2015

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Insulin is a vasoactive hormone that regulates vascular homeostasis by maintaining balance of endothelial-derived NO and ET-1. Although there is general agreement that insulin resistance and the associated hyperinsulinemia disturb this balance, the vascular consequences for hyperinsulinemia in isolation from insulin resistance are still unclear. Presently, there is no simple answer for this question, especially in a background of mixed reports examining the effects of experimental hyperinsulinemia on endothelial-mediated vasodilation. Understanding the mechanisms by which hyperinsulinemia induces vascular dysfunction is essential in advancing treatment and prevention of insulin resistance-related vascular complications. Thus, we review literature addressing the effects of hyperinsulinemia on vascular function. Furthermore, we give special attention to the vasoregulatory effects of hyperinsulinemia on skeletal muscle, the largest insulin-dependent organ in the body. This review also characterizes the differential vascular effects of hyperinsulinemia on large conduit vessels versus small resistance microvessels and the effects of metabolic variables in an effort to unravel potential sources of discrepancies in the literature. At the cellular level, we provide an overview of insulin signaling events governing vascular tone. Finally, we hypothesize a role for hyperinsulinemia and insulin resistance in the development of CVD.

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“…If so, these auxiliary properties could have important applications for patients with conditions such as hypertension, post-myocardial infarction, chronic kidney disease, heart failure and diabetes in whom elevated sympathetic activity and decreased vagal HR (heart rate) modulation are present, and are associated with increased risk of ventricular hypertrophy [52], impaired endothelium-dependent and -independent vasodilation [53][54][55], insulin resistance [56,57], arrhythmias [58] and premature mortality [59][60][61].…”

Section: Experimental Backgroundmentioning

confidence: 99%

Statins and the autonomic nervous system

Millar

Floras

2013

Clinical Science

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Statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) reduce plasma cholesterol and improve endothelium-dependent vasodilation, inflammation and oxidative stress. A 'pleiotropic' property of statins receiving less attention is their effect on the autonomic nervous system. Increased central sympathetic outflow and diminished cardiac vagal tone are disturbances characteristic of a range of cardiovascular conditions for which statins are now prescribed routinely to reduce cardiovascular events: following myocardial infarction, and in hypertension, chronic kidney disease, heart failure and diabetes. The purpose of the present review is to synthesize contemporary evidence that statins can improve autonomic circulatory regulation. In experimental preparations, high-dose lipophilic statins have been shown to reduce adrenergic outflow by attenuating oxidative stress in central brain regions involved in sympathetic and parasympathetic discharge induction and modulation. In patients with hypertension, chronic kidney disease and heart failure, lipophilic statins, such as simvastatin or atorvastatin, have been shown to reduce MNSA (muscle sympathetic nerve activity) by 12-30%. Reports concerning the effect of statin therapy on HRV (heart rate variability) are less consistent. Because of their implications for BP (blood pressure) control, insulin sensitivity, arrhythmogenesis and sudden cardiac death, these autonomic nervous system actions should be considered additional mechanisms by which statins lower cardiovascular risk.

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Effect of mild hyperisulinemia on conduit vessel endothelial function

Abstract: Physiological hyperinsulinemia has no effect on endothelium-dependent vasodilatation in conduit vessels of healthy individuals, but it induces a slight decline in endothelium-independent vasodilatation, which is entirely explained by the insulin-induced noradrenergic activation.

Cited by 10 publications

References 33 publications

Simvastatin reduces sympathetic outflow and augments endothelium-independent dilation in non-hyperlipidaemic primary hypertension

Simvastatin reduces sympathetic outflow and augments endothelium-independent dilation in non-hyperlipidaemic primary hypertension

Skeletal Muscle Vascular Function: A Counterbalance of Insulin Action

Statins and the autonomic nervous system

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