Contraction and relaxation of aortas from diabetic rats: effects of chronic anti-oxidant and aminoguanidine treatments

Archibald, V.; Cotter, Mary A.; Keegan, Alan; Cameron, Norman E.

doi:10.1007/bf00169180

Cited by 54 publications

(41 citation statements)

References 36 publications

(46 reference statements)

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“…This contrasts with previous studies that demonstrated that aminoguanidine treatment of diabetic rats improved vasodilation in the aorta [46,47]. In addition, Cartledge et al [64] have demonstrated that the formation of advanced glycation endproducts is probably responsible for the impairment of endothelialdependent penile smooth muscle relaxation seen in diabetes.…”

Section: Discussionmentioning

confidence: 65%

“…These studies suggest that vascular dysfunction is an important factor underlying nerve conduction deficits and reduced endoneurial blood flow early in the development of diabetic neuropathy. This is supported by earlier studies that demonstrated diabetesinduced impairment in vasoreactivity in the sciatic nerve is due to reduced nitric oxide mediated endothelium-dependent relaxation [37,38].In spite of the large number of studies regarding the efficacy of treatment of diabetic [46,47]. This could be due to a decrease in advanced glycation end products, which have been demonstrated to quench nitric oxide activity [48].…”

mentioning

confidence: 59%

“…In spite of the large number of studies regarding the efficacy of treatment of diabetic [46,47]. This could be due to a decrease in advanced glycation end products, which have been demonstrated to quench nitric oxide activity [48].…”

Section: Introductionmentioning

confidence: 99%

“…Recently, Keegan et al have demonstrated that treating diabetic rats with the aldose reductase inhibitor WAY121509 completely prevented the diabetes-induced decrease in acetylcholine-induced relaxation in the corpus cavernosum vascular bed [45]. In the aorta from diabetic rats Archibald et al and Ozyazgan et al have demonstrated that treatment with aminoguanidine improved the diabetes-induced decrease in vascular relaxation [46,47]. This could be due to a decrease in advanced glycation end products, which have been demonstrated to quench nitric oxide activity [48].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Treating Streptozotocin‐Induced Diabetic Rats With Sorbinil, Myo‐Inositol or Aminoguanidine on Endoneurial Blood Flow, Motor Nerve Conduction Velocity and Vascular Function of Epineurial Arterioles of the Sciatic Nerve

Coppey

Gellett

Davidson

et al. 2001

Journal of Diabetes Research

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Previously we have demonstrated that diabetes causes impairment in vascular function of epineurial vessels, which precedes the slowing of motor nerve conduction velocity. Treatment of diabetic rats with aldose reductase inhibitors, aminoguanidine or myo-inositol supplementation have been shown to improve motor nerve conduction velocity and/or decreased endoneurial blood flow. However, the effect these treatments have on vascular reactivity of epineurial vessels of the sciatic nerve is unknown. In these studies we examined the effect of treating streptozotocininduced rats with sorbinil, aminoguanidine or myo-inositol on motor nerve conduction velocity, endoneurial blood flow and endotheliumdependent vascular relaxation of arterioles that provide circulation to the region of the sciatic nerve. Treating diabetic rats with sorbinil, aminoguanidine or myo-inositol improved the reduction of endoneurial blood flow and motor nerve conduction velocity. However, only sorbinil treatment significantly improved the diabetes-induced impairment of acetylcholinemediated vasodilation of epineurial vessels of the sciatic nerve. All three treatments were efficacious in preventing the appropriate metabolic derangements associated with either activation of the polyol pathway or increased nonenzymatic glycation. In addition, sorbinil was shown to prevent the diabetes-induced decrease in lens glutathione level. However, other mark-____________________ *Corresponding author: 3 E 17 Veterans Affairs Medical Center, Iowa City, IA 52246; tel: (319) 338-0581 ext. 7629; fax: (319) 339-7025; e-mail: myorek@icva.gov Int. Jnl. Experimental Diab. Res., 3:21-36, 2002 © 2002 Taylor and Francis 1560 ers of oxidative stress were not vividly improved by these treatments. These studies suggest that sorbinil treatment may be more effective in preventing neural dysfunction in diabetes than either aminoguanidine or myoinositol.Key words: diabetes, diabetic neuropathy, endothelium, vascular reactivity, aldose reductase inhibitor, aminoguanidine INTRODUCTIONDiabetic neuropathy is a multifactorial problem likely due to the poor control of hyperglycemia. Two of these perturbations are the activation of the polyol pathway by which glucose is metabolized to sorbitol via aldose reductase contributing to an alteration in the redox balance and a decrease in myo-inositol uptake and content and an increase in non-enzymatic glycation leading to the abnormal glycation of proteins [1,2]. In animal models of diabetes prevention of these defects by treatment with aldose reductase inhibitors, aminoguanidine or supplementation with myo-inositol has been shown to improve peripheral neuropathy.Studies from numerous laboratories have shown that treating diabetic rats with an aldose reductase inhibitor improves nerve function as well as endoneurial blood flow [3][4][5][6][7][8][9][10][11][12]. This has led to wide speculation regarding the potential benefit of aldose reductase inhibitor treatment of diabetic complications [10][11][12][13][14][15][16]. However, clinical tri...

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Section: Discussionmentioning

confidence: 65%

mentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effect of Treating Streptozotocin‐Induced Diabetic Rats With Sorbinil, Myo‐Inositol or Aminoguanidine on Endoneurial Blood Flow, Motor Nerve Conduction Velocity and Vascular Function of Epineurial Arterioles of the Sciatic Nerve

Coppey

Gellett

Davidson

et al. 2001

Journal of Diabetes Research

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show abstract

“…Where measured, there was accompanying improvement in nerve perfusion and prevention of defective NOmediated endothelium dependent relaxation. Indeed, such effect was seen by treatment with butylated hydroxytoluene, a lipophilic scavenger (Archibald et al, 1996) and antioxidant effects to improve nerve blood flow and NCV in diabetic rats are blocked by cotreatment with a low dose of a NO synthase inhibitor .…”

Section: Introductionmentioning

confidence: 99%

Remedial Effects of Vitamin E and L-Arginine on Peripheral Neuropathy in Streptozotocin-Induced Diabetic Rats

Bin-Jaliah¹

2014

American Journal of Pharmacology and Toxicology

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It was shown that hyperglycemia in diabetic patients is the main factor of diabetic peripheral neuropathies. Various pathways related to oxidative stress, vascular defect and defective endothelium dependent relaxation have been implicated in the development of diabetic peripheral neuropathy. A substantial number of studies have shown that antioxidant treatment are promising therapeutics that can prevent or correct reduced motor nerve conduction in diabetic rats by acting on these mechanisms. This study was designed to investigate the possible role of insulin treatment along with or without vitamin E or L-arginine on diabetic neuropathy. This goal was accessed by examining nerve conduction, parameters of oxidative stress and lipid peroxidation as well as the expression level of endothelial nitric oxide synthase in the sciatic nerve of control and streptozotocine-induced diabetic rats. Data showed that diabetic rats showed increased levels of serum glucose (382.5%) and sciatic nerve lipid peroxidation Marker (MDA, 261.6%) with a concomitant decrease in the expression of sciatic nerve eNOS mRNA as compared to control rats. The nerve conduction studies of the sciatic nerves of these rats showed decrease conduction as evident by delayed NCV (63.6%) and low Amplitude of Muscle Contraction (AMC, 36.4%). Solitary insulin treatment (but not vitamin-E or L-arginine) corrected serum glucose to control values and corrected nerve conduction parameters in the sciatic nerve. However, treating diabetic rats with different doses of vitamin E (300 mg kg −1 and 600 mg kg −1 ) significantly reduced oxidative stress by decreasing MDA and increasing GPx activity, corrected NCV by reducing the latency and improving AMC and increased eNOS mRNA expression in sciatic nerve with a more profound effect to seen with the high dose (600 mg kg −1 ). However, the maximum potent ameliorating effect of the vitamin E on these parameters was seen when administered in combination with insulin. On the other hand, L-arginine treatment alone or in combination with insulin had no effect on the oxidative stress markers nor eNOS expression but significantly and maximally improved NCV through reducing the conduction latency and increasing AMC. This study supported the notion that diabetic peripheral neuropathy is a multifactorial complication, caused by hyperglycemia, oxidative stress and vascular impairment. It is concluded that conjugate treatment with vitamin-E, especially in higher doses, with insulin could be of great value. Moreover correction of impaired nerve blood flow by drugs that induce nitric oxide has proved to be efficient in the protection against and correction of experimental diabetic peripheral neuropathy.

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Corpus cavernosum dysfunction in diabetic rats: effects of combined α‐lipoic acid and γ‐linolenic acid treatment

Keegan

Cotter

Cameron

2001

Diabetes Metabolism Res

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Contraction and relaxation of aortas from diabetic rats: effects of chronic anti-oxidant and aminoguanidine treatments

Cited by 54 publications

References 36 publications

Effect of Treating Streptozotocin‐Induced Diabetic Rats With Sorbinil, Myo‐Inositol or Aminoguanidine on Endoneurial Blood Flow, Motor Nerve Conduction Velocity and Vascular Function of Epineurial Arterioles of the Sciatic Nerve

Effect of Treating Streptozotocin‐Induced Diabetic Rats With Sorbinil, Myo‐Inositol or Aminoguanidine on Endoneurial Blood Flow, Motor Nerve Conduction Velocity and Vascular Function of Epineurial Arterioles of the Sciatic Nerve

Remedial Effects of Vitamin E and L-Arginine on Peripheral Neuropathy in Streptozotocin-Induced Diabetic Rats

Corpus cavernosum dysfunction in diabetic rats: effects of combined α‐lipoic acid and γ‐linolenic acid treatment

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