Impaired in vivo venous constriction in conscious obese Zucker rats with metabolic syndrome

Song, Dongzhe; Hutchings, Simon; Pang, Catherine C.Y.

doi:10.1007/s00210-006-0088-8

Cited by 5 publications

(4 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since MMP/TIMP-1 in diabetic group was greatly enhanced, which may underlie the change of vascular tissue due to degradation of extracelluar matrix, then the enhancement of vasoconstriction responses to NE. These results are in accordance with previous findings that aortic vasoconstriction was augmented in a db/db mouse model [31], [32], while in contrast to the findings that vasoconstriction was impaired in vivo in metabolic syndrome rats [33], and in other arteries of STZ-induced diabetes rats [34]. The possible reason of this controversy might be that the impairment of the NOS signaling involved in aortic function in hyperinsulinimic diabetic models is much greater than that in insulin-deficient ones [35].…”

Section: Discussionsupporting

confidence: 92%

17ß-Estradiol Antagonizes the Down-Regulation of ERα/NOS-3 Signaling in Vascular Endothelial Dysfunction of Female Diabetic Rats

Han

Zhou

et al. 2012

PLoS ONE

View full text Add to dashboard Cite

Previous studies indicated that estrogen could improve endothelial function. However, whether estrogen protects vascular complications of diabetes has yet to be clarified. The study was designed to investigate the action of 17ß-estradiol on vascular endothelium in streptozotocin (STZ)-induced diabetic rats. Ovariectomized female Sprague-Dawley rats were administered with streptozotocin to produce an ovariectomized-diabetic (OVS) model which manifested as dysfunction of aortic dilation and contraction ability. Meanwhile, OVS animals with 17ß-estradiol supplementation significantly improved aortic function. Accordingly, nitric oxide synthase-3 (NOS-3), Akt, PI3K and estrogen receptor α (ERα) protein expression in aorta declined in the OVS group. Such effects were partially restored by estrogen replacement. The presence of 17ß-estradiol similarly counteracted the reduction of cyclic guanosine monophosphate (cGMP), the enhanced expression of inducible NOS (NOS-2) and NO metabolites (nitrite and nitrate), as well as the increase of matrix metalloproteinase-9/tissue inhibitor of metalloproteinase-1 (MMP-9/TIMP-1), which is an index of arterial compliance. 17ß-estradiol could also decrease ROS production in vascular endothelium. In EA hy 926 cells we found that ER antagonist, wortmannin and Akt inhibitor could block improvement effects of 17ß-estradiol. These results strongly suggest that functional impairment of the ERα/NOS-3 signaling network in OVS animals was partially restored by 17ß-estradiol administration, which provides experimental support for estrogen recruitment to improve vascular outcomes in female diabetes after endogenous hormone depletion.

show abstract

Section: Discussionsupporting

confidence: 92%

17ß-Estradiol Antagonizes the Down-Regulation of ERα/NOS-3 Signaling in Vascular Endothelial Dysfunction of Female Diabetic Rats

Han

Zhou

et al. 2012

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…Relation between obesity and hypertension is well known, but the effect of obesity on venous function is not clearly established. In an animal study, impaired in vivo venous pressor response has been shown 19 . We did not find primary influence of hypertension or hypothyroidism on the higher clinical scores of CVI in this study.…”

Section: Discussionmentioning

confidence: 98%

Correlation of obesity & comorbid conditions with chronic venous insufficiency: Results of a single-centre study

Mahapatra¹,

Ramakrishna²,

Gupta³

et al. 2018

Indian J Med Res

View full text Add to dashboard Cite

Background & objectives:Chronic venous insufficiency (CVI) is a common clinical problem among obese patients. This study was conducted to evaluate the impact of body mass index (BMI) and associated morbidities such as diabetes, hypertension and hypothyroidism on venous disease clinical scores as per Clinical, Etiological, Anatomical, Pathological (CEAP) classification.Methods:In this study, adult patients with BMI more than 30 kg/m2 with signs of CVI were evaluated clinically and by using Duplex ultrasonography of venous system. The patients with C0, C1, C2, C3 and C4, C5, C6 clinical scores in CEAP classification were grouped as lower and higher clinical scores of CVI, respectively.Results:Of the 200 enrolled patients, 147 (73.5%) were males and were associated with higher grades of clinical scores (P=0.051). Superficial venous system was involved in 96 per cent patients and 91 per cent patients had reflux in the sapheno-femoral junction. A negative association was observed between hypertension and male gender (P=0.001). Higher BMI was associated with higher clinical scoring (P=0.053). BMI >40 kg/m2 was associated with primary aetiology (P=0.007) of CVI. There was no correlation between superficial, deep or perforator incompetence with BMI (P=0.506). Duplex-confirmed significant reflux was observed in patients with higher BMI (P=0.006). Age and BMI were positively correlated with clinical score (r=0.176; P=0.013 & r=0.140; P=0.049), respectively.Interpretation & conclusions:Our findings indicated that elderly male patients with high BMI seemed to be at a higher risk of advanced clinical grades of CVI. The impact of comorbid conditions such as diabetes, hypertension and hypothyroidism on CVI could not reach at significance in the present study.

show abstract

“…Several studies have found increased α-AR vascular reactivity in isolated and anaesthetised preparations from both type 1 and type 2 diabetic (20, 30, 38) and obese models (28, 29, 37). Alternatively, some studies reported unchanged [ 18 , 21 ] or reduced [ 43 , 44 ] vascular α-AR responses. However use of low phenylephrine doses that also failed to discern a difference in our study [ 18 ] or nonspecific α-AR stimulation with noradrenaline [ 43 , 44 ], may explain these differences.…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, some studies reported unchanged [ 18 , 21 ] or reduced [ 43 , 44 ] vascular α-AR responses. However use of low phenylephrine doses that also failed to discern a difference in our study [ 18 ] or nonspecific α-AR stimulation with noradrenaline [ 43 , 44 ], may explain these differences. The present study shows augmented vascular α-AR responsiveness, in magnitude and in duration, in conscious type 2 diabetic and obese animals, at clinical doses of phenylephrine (32).…”

Section: Discussionmentioning

confidence: 99%

Increased haemodynamic adrenergic load with isoflurane anaesthesia in type 2 diabetic and obese rats in vivo

Bussey

Leeuw

Lamberts

2014

Cardiovasc Diabetol

View full text Add to dashboard Cite

BackgroundIncreasing numbers of type 2 diabetic and obese patients with enhanced rates of cardiovascular complications require surgical interventions, however they have a higher incidence of perioperative haemodynamic complications, which has been linked to adrenergic dysfunction. Therefore, we aimed to determine how α- and β-adrenoceptor (AR)-mediated haemodynamic responses are affected by isoflurane anaesthesia in experimental type 2 diabetes and obesity in vivo.MethodsSixteen-week old male Zucker type 2 Diabetic Fatty (ZDF) rats, Zucker Obese rats and their lean counterparts (n = 7-9 per group) were instrumented with radio telemeters to record blood pressure and heart rate and with vascular access ports for non-invasive intravenous drug delivery in vivo. Haemodynamic effects of α-AR (phenylephrine; 1-100 μg.kg−1) or β-AR (dobutamine; 2-120 μg.kg−1) stimulation were assessed under conscious and anaesthetised (isoflurane; 2%) conditions.ResultsVascular α-AR sensitivity was increased in both diabetic (non-diabetic 80 ± 3 vs. diabetic 95 ± 4 ΔmmHg at 100 μg.kg−1; p < 0.05) and obese (lean 65 ± 6 vs. obese 84 ± 6 ΔmmHg at 20 μg.kg−1; p < 0.05) conscious rats. Interestingly, anaesthesia exacerbated and prolonged the increased α-AR function in both diabetic and obese animals (non-diabetic 51 ± 1 vs. diabetic 68 ± 4 ΔmmHg, lean 61 ± 5 vs. obese 84 ± 2 ΔmmHg at 20 μg.kg−1; p < 0.05). Meanwhile, β-AR chronotropic sensitivity was reduced in conscious diabetic and obese rats (non-diabetic 58 ± 7 vs. diabetic 27 ± 8 Δbpm, lean 103 ± 12 vs. obese 61 ± 9 Δbpm at 15 μg.kg−1; p < 0.05). Anaesthesia normalised chronotropic β-AR responses, via either a limited reduction in obese (lean 51 ± 3 vs. obese 66 ± 5 Δbpm; NS at 15 μg.kg−1) or increased responses in diabetic animals (non-diabetic 49 ± 8 vs. diabetic 63 ± 8 Δbpm, at 15 μg.kg−1; NS at 15 μg.kg−1).ConclusionsLong term metabolic stress, such as during type 2 diabetes and obesity, alters α- and β-AR function, its dynamics and the interaction with isoflurane anaesthesia. During anaesthesia, enhanced α-AR sensitivity and normalised β-AR function may impair cardiovascular function in experimental type 2 diabetes and obesity.

show abstract

Impaired in vivo venous constriction in conscious obese Zucker rats with metabolic syndrome

Cited by 5 publications

References 42 publications

17ß-Estradiol Antagonizes the Down-Regulation of ERα/NOS-3 Signaling in Vascular Endothelial Dysfunction of Female Diabetic Rats

17ß-Estradiol Antagonizes the Down-Regulation of ERα/NOS-3 Signaling in Vascular Endothelial Dysfunction of Female Diabetic Rats

Correlation of obesity & comorbid conditions with chronic venous insufficiency: Results of a single-centre study

Increased haemodynamic adrenergic load with isoflurane anaesthesia in type 2 diabetic and obese rats in vivo

Contact Info

Product

Resources

About