ArticleBritish journal of pharmacology1994
The effects of aldose reductase inhibition with ponalrestat on changes in vascular function in streptozotocin diabetic rats.
Article in British journal of pharmacology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 37 citations in OpenAlex.
- Sexual dimorphism in rat aortic endothelial function of streptozotocin-induced diabetes: possible involvement of superoxide and nitric oxide production.European journal of pharmacology · 2014Article
- Effects of streptozotocin-induced diabetes on the pharmacology of rat conduit and resistance intrapulmonary arteries.Cardiovascular diabetology · 2009Article
- Impairment of endothelium- and nerve-mediated relaxation responses in the cavernosal smooth muscle of experimentally diabetic rabbits: role of weight loss and duration of diabetes.Naunyn-Schmiedeberg's archives of pharmacology · 2006Article
- Endothelial dysfunction in diabetes.British journal of pharmacology · 2000Review
- Comparison of the effects of ascorbyl gamma-linolenic acid and gamma-linolenic acid in the correction of neurovascular deficits in diabetic rats.Diabetologia · 1996Article
- Contraction and relaxation of aortas from diabetic rats: effects of chronic anti-oxidant and aminoguanidine treatments.Naunyn-Schmiedeberg's archives of pharmacology · 1996Article
- Interactions between essential fatty acid, prostanoid, polyol pathway and nitric oxide mechanisms in the neurovascular deficit of diabetic rats.Diabetologia · 1996Article
- Chronic vitamin E treatment prevents defective endothelium-dependent relaxation in diabetic rat aorta.Diabetologia · 1995Article
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2 authors at 1 institution in 1 country.
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Abstract
1. The responses of rat isolated aortae to vasoconstrictor and vasodilator agents have been studied in 14-day streptozotocin-diabetic rats. The effects of treatment with the aldose reductase inhibitor, ponalrestat, on these responses have also been investigated. 2. Maximum contractile responses and aortic sensitivity to phenylephrine were significantly enhanced in 14-day diabetic aortae. 3. In contrast, endothelium-dependent relaxations to carbachol were depressed in diabetic rats, whilst endothelium-independent relaxations to forskolin and sodium nitroprusside were unchanged. 4. Pretreatment with ponalrestat (25 mg kg-1, daily) prevented both the enhanced maximum contractile responses to phenylephrine and the depressed endothelium-dependent relaxations to carbachol in aortae from 14-day diabetic rats. Ponalrestat however, had no effect on the reduced phenylephrine EC50 values observed in tissues from diabetic animals. 5. It is concluded that ponalrestat prevents the depression of endothelium-dependent aortic relaxations induced by diabetes of 14 days duration, suggesting that the polyol pathway is involved in these vascular changes. Ponalrestat does not prevent the increase in aortic sensitivity to alpha 1-adrenoceptor agonists.
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