Modulation of Vascular Reactivity by Perivascular Adipose Tissue (PVAT)

Agabiti-Rosei, Claudia; Paini, Anna; Ciuceis, Carolina De; Withers, Sarah; Greenstein, Adam; Heagerty, Anthony M.; Rizzoni, Damiano

doi:10.1007/s11906-018-0835-5

Cited by 40 publications

(46 citation statements)

References 93 publications

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“…This finding reaffirmed the idea that PVAT was anti-contractile. Since this study, investigators have reproduced that the presence of PVAT in healthy tissue is 'anti-contractile' [5][6][7][8][9][10][11] . Gollasch uses the term "adipose-vascular coupling" for the interaction of PVAT with the vessel 12 and, in health, this coupling is beneficial.…”

mentioning

confidence: 75%

A New Function for Perivascular Adipose Tissue (PVAT): Assistance of Arterial Stress Relaxation

Watts

Flood

Garver

et al. 2020

Sci Rep

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in health, pVAt secretes anti-contractile factors that relax the underlying artery. pVAt's contributions to vascular function include more than production of vasoactive substances. We hypothesized that PVAT benefits the artery by assisting the function of stress (-induced) relaxation. Thoracic aorta rings from Sprague Dawley rats were mounted in isolated tissue baths with (+) and without (−) PVAT. A cumulative length tension (0-6 grams) was generated. The tension to which the tissue stress relaxed over 30 minutes was recorded; the tension lost was stress relaxation. The presence of PVAT increased the amount of stress relaxation (final tension in mgs; aortic ring −pVAt = 4578 ± 190; aortic ring + pVAt = 2730 ± 274, p < 0.05). PVAT left attached but not encompassing the aorta provided no benefit in cumulative stress relaxation (aortic ring +/− pVAt = 4122 ± 176; p > 0.05 vs −pVAt). A pVAt ring separated from the aorta demonstrated more profound stress relaxation than did the aortic ring itself. finally, pVAt-assisted stress relaxation was observed in an artery with white fat (superior mesenteric artery) and in aorta from both male and female of another rat strain, the Dahl S rat. Knowledge of this new pVAt function supports pVAt as an essential player in vascular health.

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mentioning

confidence: 75%

A New Function for Perivascular Adipose Tissue (PVAT): Assistance of Arterial Stress Relaxation

Watts

Flood

Garver

et al. 2020

Sci Rep

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“…PVAT is a secretory organ involved in the regulation of hemodynamic homeostasis, and a balance between PVAT-derived vasodilator and vasoconstrictor mediators appears to be important to maintain an appropriate vascular tone [ 3 , 4 ]. Even when the volume of PVAT is associated with hypertension and aortic and coronary calcification, it is the function of PVAT, rather than the size of this tissue, which seems to be key for the control of vascular homeostasis [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

“…Apart from the visceral and subcutaneous fat depots, numerous blood vessels are surrounded by a specific type of adipose tissue termed perivascular adipose tissue (PVAT). Increasing evidence demonstrates that PVAT acts as a secretory and endocrine organ with a direct impact on vessel function, structure, and contractility [ 3 ]. In addition to adipocytes, other cell types, such as macrophages, lymphocytes, and fibroblasts, are found in PVAT and may also contribute to its function.…”

Section: Introductionmentioning

confidence: 99%

Myeloid GRK2 Regulates Obesity-Induced Endothelial Dysfunction by Modulating Inflammatory Responses in Perivascular Adipose Tissue

et al. 2020

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Perivascular adipose tissue (PVAT) is increasingly being regarded as an important endocrine organ that directly impacts vessel function, structure, and contractility in obesity-associated diseases. We uncover here a role for myeloid G protein-coupled receptor kinase 2 (GRK2) in the modulation of PVAT-dependent vasodilation responses. GRK2 expression positively correlates with myeloid- (CD68) and lymphoid-specific (CD3, CD4, and CD8) markers and with leptin in PVAT from patients with abdominal aortic aneurysms. Using mice hemizygous for GRK2 in the myeloid lineage (LysM-GRK2+/−), we found that GRK2 deficiency in myeloid cells allows animals to preserve the endothelium-dependent acetylcholine or insulin-induced relaxation, which is otherwise impaired by PVAT, in arteries of animals fed a high fat diet (HFD). Downregulation of GRK2 in myeloid cells attenuates HFD-dependent infiltration of macrophages and T lymphocytes in PVAT, as well as the induction of tumor necrosis factor-α (TNFα) and NADPH oxidase (Nox)1 expression, whereas blocking TNFα or Nox pathways by pharmacological means can rescue the impaired vasodilator responses to insulin in arteries with PVAT from HFD-fed animals. Our results suggest that myeloid GRK2 could be a potential therapeutic target in the development of endothelial dysfunction induced by PVAT in the context of obesity.

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“…The anti-contractile effect of perivascular adipose tissue (PVAT) is lost in obesity, probably as a consequence of the development of adipocyte hypertrophy, inflammation, and oxidative stress thus contributing to endothelial dysfunction observed inobesity and hypertension. Thus, decreased local adiponectin level, macrophage recruitment and infiltration, and activation of renin-angiotensin-aldosterone system could play an important role in hypertension 30 . The patho-physiological links between obesity mediated diabetes and hypertension is another important mechanism.…”

Section: Obesity and Hypertensionmentioning

confidence: 99%

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2018

IJPSR

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Obesity is the primary cause of metabolic syndrome (MS), further developing to atherosclerosis, hypertension, insulin resistance and diabetes in different individuals depending on their predisposed genetic background. Though adipose tissue acts as endocrine gland, as storage for energy reserve and insulation to vital organs but overloaded adipose tissue, turns inflammatory and induces systemic low grade inflammation (LGI), affecting the normal physiology. The endothelial cells, the innermost layer of a blood vessel, are the most affected ones and responsible for micro and macro-vascular complications. Obesity is linked to dysfunction of endoplasmic reticulum and mitochondria in variety of cells resulting oxidative stress, accumulation of residual damaged cell organelles and ER stress leading to UPRs (unfolded protein responses) accumulation in the cytoplasm. This is also associated to low autophagy. The whole process activates the innate immunity and attracts macrophages towards adipose tissue and secretes abnormal adipokines and inflammatory cytokines. At physiological level it is manifested as changed neurological secretions, sleep pattern, appetite, and hunger signals. Thus, activation of antioxidant enzymes and autophagy by changed life style (sleep cycle resonance with circadian rhythm), regulation of digestive power and food habits (energy intake/expenditure balance), medicinal supplements (medicine and herbal) and behavioural changes (psychological and environmental factors) may prove effective in management of obesity and related complications. Here, we have discussed the etiological factors responsible behind the pathogenesis of MS and involved signaling pathways with reference to autophagy. INTRODUCTION: Obesity is a public health problem with continuous rising trend. In 2010, overweight and obese persons were estimated to cause 3.4 million deaths, 3.9% of years of life lost, and 3.8% of DALYs (disability adjusted life years) globally 1. Another study of 2015 indicates that, a total of 107.7 million children and 603.7 million adults were obese. High BMI accounted for 4.0 million deaths globally and its 40% occurred in persons who were not obese.

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Modulation of Vascular Reactivity by Perivascular Adipose Tissue (PVAT)

Cited by 40 publications

References 93 publications

A New Function for Perivascular Adipose Tissue (PVAT): Assistance of Arterial Stress Relaxation

A New Function for Perivascular Adipose Tissue (PVAT): Assistance of Arterial Stress Relaxation

Myeloid GRK2 Regulates Obesity-Induced Endothelial Dysfunction by Modulating Inflammatory Responses in Perivascular Adipose Tissue

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