Metabolic syndrome and endothelin-1 mediated vasoconstrictor tone in overweight/obese adults

Rocha, Nazareth de Novaes; Templeton, Danielle L.; Greiner, Jared J.; Stauffer, Brian L.; DeSouza, Christopher A.

doi:10.1016/j.metabol.2014.04.007

Cited by 19 publications

(15 citation statements)

References 37 publications

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“…For example, Schinzari, et al (Schinzari et al 2015) demonstrated that endothelium-dependent vasodilator dysfunction is worse in obese adults with MetS than obese adults without MetS. Moreover, we recently demonstrated (Rocha et al 2014) that MetS is associated with higher endothelin-1-mediated vasoconstrictor tone in obese adults. The results of the present study significantly extend these findings by demonstrating that endotheliumdependent vasodilation is markedly reduced in normal weight adults with MetS.…”

Section: Discussionmentioning

confidence: 59%

“…The mechanisms underlying the D r a f t increased CV risk with MetS are not fully understood, but endothelial dysfunction is considered a primary contributing factor (Suzuki et al 2008). In obese adults with MetS, endothelial vasomotor function, a key feature of endovascular health, is negatively affected (Schinzari et al 2010;Rocha et al 2014;Schinzari et al 2015). For example, Schinzari, et al (Schinzari et al 2015) demonstrated that endothelium-dependent vasodilator dysfunction is worse in obese adults with MetS than obese adults without MetS.…”

Section: Discussionmentioning

confidence: 99%

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Endothelial vasodilator function in normal-weight adults with metabolic syndrome

Dow

Lincenberg

Greiner

et al. 2016

Appl. Physiol. Nutr. Metab.

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Metabolic syndrome (MetS) typically presents with obesity; however, obesity is not a requisite characteristic for MetS classification and related vascular risk. We tested the hypothesis that MetS, independent of excess adiposity, is associated with impaired endothelial vasodilator dysfunction. Thirty-two sedentary, middle-aged adults were studied: 11 normal weight (9 male and 2 female; body mass index (BMI), 24.0 ± 0.3 kg/m); 11 normal weight with MetS (9 male and 2 female; BMI, 24.7 ± 0.3 kg/m); and 10 obese without MetS (8 male and 2 female; BMI, 31.4 ± 0.5 kg/m). MetS was established according to National Cholesterol Education Program Adult Treatment Panel III criteria. Forearm blood flow (FBF) responses to intra-arterial infusions of acetylcholine and sodium nitroprusside were measured via strain-gauge plethysmography. FBF responses to acetylcholine were ∼20% lower (P < 0.05) in the normal-weight subjects with MetS (from 4.0 ± 0.3 to 13.0 ± 1.0 mL/(100 mL tissue·min)) and obese subjects (from 4.8 ± 0.2 to 12.2 ± 1.1 mL/(100 mL tissue·min)) compared with the normal-weight subjects (from 4.6 ± 0.4 to 15.8 ± 0.7 mL/(100 mL tissue·min)). Of note, FBF responses to acetylcholine were similar between the normal-weight adults with MetS and the obese adults. There were no differences among groups in FBF response to sodium nitroprusside. These data indicate that the presence of MetS, independent of obesity, is associated with diminished endothelium-dependent vasodilation. Endothelial vasodilator dysfunction may underlie the increased cardiovascular risk in normal-weight adults with MetS.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Endothelial vasodilator function in normal-weight adults with metabolic syndrome

Dow

Lincenberg

Greiner

et al. 2016

Appl. Physiol. Nutr. Metab.

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“…The prominent role for obesity fits into a recently proposed paradigm whereby metabolic co‐morbidities drive LV remodelling and dysfunction in HFPEF and into earlier observations that metabolic syndrome reinforces pulmonary venous hypertension . The former was explained by deficient myocardial microvascular nitric oxide (NO)/cGMP signalling, and the latter by excessive pulmonary venous endothelin‐1‐mediated vasoconstrictor tone . Both derive from a deranged Yin–Yang between endothelial NO and endothelin‐1 in metabolic disturbances .…”

Section: Characteristics Of the Misclassified Pulmonary Hypertension mentioning

confidence: 72%

“…11 The former was explained by deficient myocardial microvascular nitric oxide (NO)/cGMP signalling, 12 and the latter by excessive pulmonary venous endothelin-1-mediated vasoconstrictor tone. 13 Both derive from a deranged Yin-Yang between endothelial NO and endothelin-1 in metabolic disturbances. 14 The clinical characteristics of the misclassified PHT provide the readers of the journal with an important 'take-home' message, namely that overweight/obese patients with PHT and normal PAWP need to undergo invasive exercise testing or a volume infusion challenge before they can be classified as pre-capillary PHT group 1 patients.…”

Section: Characteristics Of the Misclassified Pulmonary Hypertension mentioning

confidence: 99%

Normal resting pulmonary artery wedge pressure: a diagnostic trap for heart failure with preserved ejection fraction

Franssen

Paulus

2015

European J of Heart Fail

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This article refers to 'Exercise haemodynamics may unmask the diagnosis of diastolic dysfunction among patients with pulmonary hypertension' by E. Maor et al., published in this issue on page 151The diagnosis of heart failure with preserved ejection fraction (HFPEF) remains challenging. A correct diagnosis requires the presence of signs or symptoms of congestion, normal LV systolic function, and evidence of diastolic LV dysfunction.1 Failure to establish the diagnosis of HFPEF correctly can be related to omission of evidence of diastolic LV dysfunction, 2 to exclusive reliance on elevated natriuretic peptides, 3 which are only modestly raised in HFPEF, 4 and to the fortuitous presence of a hypovolaemic status at the time of diagnostic evaluation, 5 which necessitates a repeat assessment during exercise 6 or saline infusion. 7 The latter was convincingly demonstrated in the current issue of the journal by the study of Maor et al., who performed a limited upper body exercise stress test mimicking daily living activities during right heart catheterization in patients with pulmonary hypertension (PHT) [mean pulmonary artery pressure (mPAP) >25 mmHg] and normal resting pulmonary artery wedge pressure (PAWP <15 mmHg). 8Despite attaining a rise in heart rate of 10%, which was only 62% of the age-predicted maximal heart rate, one-third of the patients had a substantial rise of PAWP from 11.4 ± 3.3 to 28.0 ± 6.5 mmHg. Without exercise stress testing, their HFPEF-induced post-capillary (group 2) PHT would have remained unnoticed and these patients would have been erroneously classified as pre-capillary (group 1) PHT in accordance with the Dana Point PHT criteria. 9 Significant predictors of an exercise-induced rise in PAWP were a borderline resting PAWP (12 < PAWP < 15 mmHg), a high body mass index (BMI), presence of obesity, and a dilated left atrium.

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“…Hypertension, a disorder associated with structural and functional vascular alterations, has been recognized as a major risk to cardiovascular health (1). As hypertension is correlated with coronary artery disease, left ventricular hypertrophy, congestive heart failure, obesity, hyperlipidemia, diabetes and cerebrovascular complications, it represents the biggest single contributor to the global burden of disease and to global mortality (1)(2)(3)(4). Recent studies have demonstrated that some gene variants may be involved in hypertension (2,3).…”

Section: Introductionmentioning

confidence: 99%

TRPM8 downregulation by angiotensin II in vascular smooth muscle cells is involved in hypertension

Huang

Zhang

et al. 2017

Molecular Medicine Reports

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Angiotensin II (Ang II)-induced injury of vascular smooth muscle cells (VSMCs) serves an important role in hypertension and other cardiovascular disorders. Transient receptor potential melastatin 8 (TRPM8) is a thermally‑regulated Ca2+‑permeable channel that is activated by reduced body temperature. Although several recent studies have revealed the regulatory effect of TRPM8 in vascular tone and hypertension, the precise role of TRPM8 in dysfunction of vascular smooth muscle cells (VSMCs) induced by Ang II remains elusive. In the present study, the possible function of TRPM8 in Ang II‑induced VSMCs malfunction in vivo and in vitro was investigated. In the aortae from rats that had undergone a two‑kidney one‑clip operation, which is a widely‑used renovascular hypertension model, the mRNA and protein levels of TRPM8 were reduced. In addition, exogenous Ang II treatment decreased TRPM8 mRNA and protein expression levels in primary cultures of rat VSMCs. TRPM8 activation by menthol, a pharmacological agonist, in VSMCs, significantly attenuated the Ang II‑induced increase in reactive oxygen species and H2O2 production. In addition, TRPM8 activation reduced the Ang II‑induced upregulation of NADPH oxidase (NOX) 1 and NOX4 in VSMCs. Furthermore, TRPM8 activation relieved the Ang II‑induced activation of ras homolog gene family, member A‑rho associated protein kinase 2 and janus kinase 2 signaling pathways in VSMCs. In conclusion, the results presented in the current study indicated that TRPM8 downregulation by Ang II in VSMCs may be involved in hypertension.

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Metabolic syndrome and endothelin-1 mediated vasoconstrictor tone in overweight/obese adults

Cited by 19 publications

References 37 publications

Endothelial vasodilator function in normal-weight adults with metabolic syndrome

Endothelial vasodilator function in normal-weight adults with metabolic syndrome

Normal resting pulmonary artery wedge pressure: a diagnostic trap for heart failure with preserved ejection fraction

TRPM8 downregulation by angiotensin II in vascular smooth muscle cells is involved in hypertension

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