Attenuation of the anti-contractile effect of cooling in the rat aorta by perivascular adipose tissue

2017 ◽  
Vol 37 (4) ◽  
pp. 52-60
Author(s):  
Y. Rafique ◽  
M. AlBader ◽  
M. Oriowo
Keyword(s):  
Adipose Tissue ◽  
Rat Aorta ◽  
Perivascular Adipose Tissue ◽  
Contractile Effect

scholarly journals Restoring Perivascular Adipose Tissue Function in Obesity Using Exercise

2021 ◽  
Author(s):  
Sophie N Saxton ◽  
Lauren K Toms ◽  
Robert G Aldous ◽  
Sarah B Withers ◽  
Jacqueline Ohanian ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Contractile Function ◽  
Ex Vivo ◽  
Vascular Complications ◽  
Electrical Field Stimulation ◽  
Organic Cation Transporter ◽  
Nervous Stimulation ◽  
Perivascular Adipose Tissue ◽  
Contractile Effect ◽  
Organic Cation Transporter 3

AbstractPurposePerivascular adipose tissue (PVAT) exerts an anti-contractile effect which is vital in regulating vascular tone. This effect is mediated via sympathetic nervous stimulation of PVAT by a mechanism which involves noradrenaline uptake through organic cation transporter 3 (OCT3) and β3-adrenoceptor-mediated adiponectin release. In obesity, autonomic dysfunction occurs, which may result in a loss of PVAT function and subsequent vascular disease. Accordingly, we have investigated abnormalities in obese PVAT, and the potential for exercise in restoring function.MethodsVascular contractility to electrical field stimulation (EFS) was assessed ex vivo in the presence of pharmacological tools in ±PVAT vessels from obese and exercised obese mice. Immunohistochemistry was used to detect changes in expression of β3-adrenoceptors, OCT3 and tumour necrosis factor-α (TNFα) in PVAT.ResultsHigh fat feeding induced hypertension, hyperglycaemia, and hyperinsulinaemia, which was reversed using exercise, independent of weight loss. Obesity induced a loss of the PVAT anti-contractile effect, which could not be restored via β3-adrenoceptor activation. Moreover, adiponectin no longer exerts vasodilation. Additionally, exercise reversed PVAT dysfunction in obesity by reducing inflammation of PVAT and increasing β3-adrenoceptor and OCT3 expression, which were downregulated in obesity. Furthermore, the vasodilator effects of adiponectin were restored.ConclusionLoss of neutrally mediated PVAT anti-contractile function in obesity will contribute to the development of hypertension and type II diabetes. Exercise training will restore function and treat the vascular complications of obesity.

Abstract P271: Delineating Sex-specific Mechanisms Of Impaired Vasoreactivity In Thermoneutrality

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Ji Hye Chun ◽  
Melissa M Henckel ◽  
Leslie A Knaub ◽  
Lori A Walker ◽  
Jane E Reusch ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mitochondrial Respiration ◽  
Rat Aorta ◽  
Female Rats ◽  
Ex Situ ◽  
Dependent Manner ◽  
Perivascular Adipose Tissue ◽  
Male And Female ◽  
Male And Female Rats ◽  
Brown Adipose

Cardiovascular disease (CVD) is a leading cause of hospitalization and death. CVD is characterized by impaired vasoreactivity and mitochondrial dysfunction. Perivascular adipose tissue (PVAT), considered brown adipose tissue (BAT), surrounds the vasculature and regulates its response. Preliminary data with rats housed at either their thermoneutrality (TN, 30°C) or room temperature (RT, 22°C) showed diminished vasodilation in aorta from TN rats as compared with those from RT rats (10.2% ± 4.0% (0.159 g of vasodilation capacity, starting from maximal force constriction of 1.563 g) versus 64.2% ± 5.3% (0.909 g of 1.417 g, p<0.001). TN-housed rat aorta also showed less mitochondrial respiration with lipid substrates in multiple states (p<0.05). We hypothesize that remodeling of PVAT phenotype from BAT to white adipose tissue (WAT) may alter mitochondrial lipid utilization and cause vasoreactivity dysfunction. To test this, we housed male and female rats at either RT or TN and investigated their own PVAT + aorta or PVAT from the oppositely- housed animals along with each rat’s own aorta for vasoreactivity ex situ. There was diminished vasodilation in all TN animals with PVAT + aorta (29.2% ± 3.8% (0.269 g of 0.923 g) versus 37.6% ± 6.0% (0.255 g of 0.677 g), p<0.02), with only male animals showing a significant effect from PVAT (p<0.001). In aorta of TN-housed animals analyzed with PVAT from RT-housed animals, female vessels showed an increase in vasodilation capacity as compared to controls (56.8% ± 13.6% (0.589 g of 1.037 g) versus 5.2% ± 2.3% (0.028 g of 0.534 g), p<0.001), strongly suggesting that PVAT not only regulates vasoreactivity, but can repair TN-induced diminished dilation in a sex-dependent manner. All animals at TN had significantly less mitochondrial respiration with lipid substrates (p<0.05), with no sex differences. We further observed a significantly greater amount of lipids in PVAT from male TN-housed animals as compared to that in RT-housed animals (p<0.05), consistent with a WAT phenotype. Our data support that TN alters PVAT phenotype in a sex-dependent manner, resulting in dysfunctional vasoreactivity and mitochondrial function. These targets of CVD in both male and female animals are exciting avenues for novel therapeutics.

scholarly journals Loss of anti-contractile effect of perivascular adipose tissue in offspring of obese rats

2016 ◽  
Vol 40 (8) ◽  
pp. 1205-1214 ◽  
Author(s):  
K E Zaborska ◽  
M Wareing ◽  
G Edwards ◽  
C Austin
Keyword(s):  
Adipose Tissue ◽  
Maternal Obesity ◽  
Later Life ◽  
Independent Effect ◽  
Sprague Dawley ◽  
Response Curves ◽  
Perivascular Adipose Tissue ◽  
Contractile Effect ◽  
Sprague Dawley Rats ◽  
Pregnancy And Lactation

Abstract Rationale: Maternal obesity pre-programmes offspring to develop obesity and associated cardiovascular disease. Perivascular adipose tissue (PVAT) exerts an anti-contractile effect on the vasculature, which is reduced in hypertension and obesity. Objective: The objective of this study was to determine whether maternal obesity pre-programmes offspring to develop PVAT dysfunction in later life. Methods: Female Sprague–Dawley rats were fed a diet containing 10% (control) or 45% fat (high fat diet, HFD) for 12 weeks prior to mating and during pregnancy and lactation. Male offspring were killed at 12 or 24 weeks of age and tension in PVAT-intact or -denuded mesenteric artery segments was measured isometrically. Concentration–response curves were constructed to U46619 and norepinephrine. Results: Only 24-week-old HFD offspring were hypertensive (P<0.0001), although the anti-contractile effect of PVAT was lost in vessels from HFD offspring of each age. Inhibition of nitric oxide (NO) synthase with 100 μM l-NMMA attenuated the anti-contractile effect of PVAT and increased contractility of PVAT-denuded arteries (P<0.05, P<0.0001). The increase in contraction was smaller in PVAT-intact than PVAT-denuded vessels from 12-week-old HFD offspring, suggesting decreased PVAT-derived NO and release of a contractile factor (P<0.07). An additional, NO-independent effect of PVAT was evident only in norepinephrine-contracted vessels. Activation of AMP-activated kinase (with 10 μM A769662) was anti-contractile in PVAT-denuded (P<0.0001) and -intact (P<0.01) vessels and was due solely to NO in controls; the AMPK effect was similar in HFD offspring vessels (P<0.001 and P<0.01, respectively) but was partially NO-independent. Conclusions: The diminished anti-contractile effects of PVAT in offspring of HFD dams are primarily due to release of a PVAT-derived contractile factor and reduced NO bioavailability.

Effect of high free fatty acids on the anti-contractile response of perivascular adipose tissue in rat aorta

2013 ◽  
Vol 63 ◽  
pp. 169-174 ◽  
Author(s):  
Xiaodong Sun ◽  
Ningning Hou ◽  
Fang Han ◽  
Ying Guo ◽  
Zongguang Hui ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Contractile Response ◽  
Rat Aorta ◽  
Perivascular Adipose Tissue

scholarly journals Mechanisms of Perivascular Adipose Tissue Dysfunction in Obesity

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Maria S. Fernández-Alfonso ◽  
Marta Gil-Ortega ◽  
Concha F. García-Prieto ◽  
Isabel Aranguez ◽  
Mariano Ruiz-Gayo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Vascular Function ◽  
Rat Aorta ◽  
Inflammatory Factors ◽  
Perivascular Adipose Tissue ◽  
Functional Changes ◽  
Structural Support ◽  
Diet Induced Obesity ◽  
Adipose Tissue Dysfunction ◽  
First Time

Most blood vessels are surrounded by adipose tissue. Similarly to the adventitia, perivascular adipose tissue (PVAT) was considered only as a passive structural support for the vasculature, and it was routinely removed for isolated blood vessel studies. In 1991, Soltis and Cassis demonstrated for the first time that PVAT reduced contractions to noradrenaline in rat aorta. Since then, an important number of adipocyte-derived factors with physiological and pathophysiological paracrine vasoactive effects have been identified. PVAT undergoes structural and functional changes in obesity. During early diet-induced obesity, an adaptative overproduction of vasodilator factors occurs in PVAT, probably aimed at protecting vascular function. However, in established obesity, PVAT loses its anticontractile properties by an increase of contractile, oxidative, and inflammatory factors, leading to endothelial dysfunction and vascular disease. The aim of this review is to focus on PVAT dysfunction mechanisms in obesity.

Role of Extracellular Calcium and Calcium Sensitization in the Anti-Contractile Effect of Perivascular Adipose Tissue in Pregnant Rat Aorta

Pharmacology ◽  
2019 ◽  
Vol 104 (5-6) ◽  
pp. 359-367 ◽  
Author(s):  
Aishah Al-Jarallah ◽  
Elsie Oommen ◽  
Lilly Chacko Verghese ◽  
Mabayoje A. Oriowo
Keyword(s):  
Adipose Tissue ◽  
Inhibitory Effect ◽  
Extracellular Calcium ◽  
Pregnant Rats ◽  
Perivascular Adipose Tissue ◽  
Pregnant Rat ◽  
Calcium Sensitization ◽  
Contractile Effect ◽  
Significant Difference ◽  
Gf 109203X

Previous studies have shown that the anti-contractile effect of the perivascular adipose tissue (PVAT) is attenuated in pregnancy. In the present investigation, we have examined the possibility that this loss of anti-contractile effect could be due to changes in calcium mobilization. PVAT exerted anti-contractile effect against 5-hydroxytryptamine (5-HT)-induced contractions of aorta segments from pregnant and non-pregnant rats and this anti-contractile effect was attenuated in segments from pregnant rats. Nifedipine (10–6 mol/L), an inhibitor of L-type dihydropyridine calcium channels, significantly reduced 5-HT-induced contraction of aorta segments from non-pregnant and pregnant rats with and without PVAT. The inhibitory effect of nifedipine against 5-HT-induced contractions was attenuated in PVAT-free aorta segments from pregnant rats. However, while PVAT reduced the effectiveness of nifedipine in aorta segments from non-pregnant rats, it partially restored the inhibitory effect of nifedipine in aorta segments from pregnant rats. Inhibitors of calcium sensitization, Y-27632 (10–6 mol/L) and GF 109203X (10–6 mol/L), significantly reduced 5-HT-induced contractions of PVAT-free aorta segments from non-pregnant and pregnant rats. Both inhibitors, however, were less effective in aorta segments from pregnant rats. The presence of PVAT reduced the effectiveness of Y-27632 and GF 109203X in aorta segments from pregnant and non-pregnant rats. Protein expression of Rho-associated protein kinase (ROCK) I and II was detected in aorta segments and PVAT from pregnant and non-pregnant rats. There was a reduction in the expression of both isoforms in aorta segments but not PVAT from pregnant rats. In addition, there was no significant difference in the expression of ROCK-I and ROCK-II in PVAT from pregnant and non-pregnant rats. We concluded that the loss of anti-contractile effect of PVAT in aorta segments from pregnant rats could be due to increased influx of extracellular calcium through nifedipine-sensitive dihydropyridine channels.

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