ArticleBritish journal of pharmacology1999
Effect of insulin treatment on smooth muscle contractility and endothelium-dependent relaxation in rat aortae from established STZ-induced diabetes.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 57 citations in OpenAlex.
- Engineering etiology-aligned in vitro models of human vessels.Microsystems & nanoengineering · 2026Review
- Genipin and insulin combined treatment improves implant osseointegration in type 2 diabetic rats.Journal of orthopaedic surgery and research · 2021Article
- In Vivo Effects of Quercetin in Association with Moderate Exercise Training in Improving Streptozotocin-Induced Aortic Tissue Injuries.Molecules (Basel, Switzerland) · 2015Article
- Role of ROCK upregulation in endothelial and smooth muscle vascular functions in diabetic rat aorta.Cardiovascular diabetology · 2013Article
- Article
- Diabetic state, high plasma insulin and angiotensin II combine to augment endothelin-1-induced vasoconstriction via ETA receptors and ERK.British journal of pharmacology · 2008Article
- Early diabetic neuropathy: triggers and mechanisms.World journal of gastroenterology · 2007Review
- Possible involvement of IGF-1 receptor and IGF-binding protein in insulin-induced enhancement of noradrenaline response in diabetic rat aorta.British journal of pharmacology · 2003Article
- Relationship between peroxisome proliferator-activated receptors (PPAR alpha and PPAR gamma) and endothelium-dependent relaxation in streptozotocin-induced diabetic rats.British journal of pharmacology · 2003Article
- Hyper-reactivity of diacylglycerol kinase is involved in the dysfunction of aortic smooth muscle contractility in streptozotocin-induced diabetic rats.British journal of pharmacology · 2002Article
- Effects of chronic administration of the novel endothelin antagonist J-104132 on endothelial dysfunction in streptozotocin-induced diabetic rat.British journal of pharmacology · 2002Article
- Effects of diabetes on neurotransmission in rat vaginal smooth muscle.International journal of impotence research · 2001Article
- The effect of long-term streptozotocin-induced diabetes on contractile and relaxation responses of coronary arteries: selective attenuation of CGRP-induced relaxations.British journal of pharmacology · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. This study involved the chronic administration of low or high insulin to rats with established streptozotocin (STZ)-induced diabetes. We studied the effect of such treatment on smooth muscle contractility and endothelium-dependent relaxation using aortic strips. 2. Aortae from diabetic rats, but not those from high-insulin-treated diabetic rats, showed an impaired endothelium-dependent in response to acetylcholine (ACh) by comparison with untreated controls. 3. Isotonic high K+-induced contractility was impaired in diabetic aortae. This impairment was prevented by high-insulin treatment. 4. Noradrenaline (NA)-induced contractility was enhanced in aortae from high-insulin-treated diabetic rats, but not in those from untreated diabetic or low-insulin treated diabetic rats. 5. In the combined presence of the nitric oxide inhibitor N(G)-nitro-L-arginine and the cyclo-oxygenase inhibitor indomethacin, NA-induced contractility was significantly greater in aortae from high-insulin-treated diabetic rats than in those from controls or untreated diabetic rats. 6. An increased expression of the mRNA for the alpha1D and alpha1B adrenergic receptors was found in aortae from high-insulin-treated diabetic rats. 7. These results demonstrate that in rats with established STZ-induced diabetes, high-insulin treatment prevents the development of an impaired endothelium-dependent relaxation in the aorta, and that such treatment enhances NA-induced contractility. This enhancement may be related to an upregulation in the expression of the mRNA for the alpha1B or alpha1D adrenergic receptor that is secondary to the hyperinsulinaemia.
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