ArticleBritish journal of pharmacology2000
Mechanisms underlying the attenuation of endothelium-dependent vasodilatation in the mesenteric arterial bed of the streptozotocin-induced diabetic rat.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Potassium supplementation and depletion during development of salt-sensitive hypertension in male and female SS rats.JCI insight · 2025Article
- 17β-Estradiol Treatment Improves Acetylcholine-Induced Relaxation of Mesenteric Arteries in Ovariectomized UC Davis Type 2 Diabetes Mellitus Rats in Prediabetic State.Frontiers in physiology · 2022Article
- Chronic Inhibition of mROS Protects Against Coronary Endothelial Dysfunction in Mice With Diabetes.Frontiers in cell and developmental biology · 2021Article
- Article
- Diabetes Attenuates the Contribution of Endogenous Nitric Oxide but Not Nitroxyl to Endothelium Dependent Relaxation of Rat Carotid Arteries.Frontiers in pharmacology · 2020Article
- Endothelium-Dependent Hyperpolarization (EDH) in Diabetes: Mechanistic Insights and Therapeutic Implications.International journal of molecular sciences · 2019Review
- Vasoactive actions of nitroxyl (HNO) are preserved in resistance arteries in diabetes.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Blockade of sigma 1 receptors alleviates sensory signs of diabetic neuropathy in rats.European journal of pain (London, England) · 2017Article
- Recombinant PAI-1 therapy restores myoendothelial junctions and erectile function in PAI-1-deficient mice.Andrologia · 2015Article
- The role of epoxyeicosatrienoic acids in the cardiovascular system.British journal of clinical pharmacology · 2015Review
- Treadmill running improves hindlimb arteriolar endothelial function in type 1 diabetic mice as visualized by X-ray microangiography.Cardiovascular diabetology · 2015Article
- Article
- Sex-specific alterations in NOS regulation of vascular function in aorta and mesenteric arteries from spontaneously hypertensive rats compared to Wistar Kyoto rats.Physiological reports · 2014Article
- Sex differences in mesenteric endothelial function of streptozotocin-induced diabetic rats: a shift in the relative importance of EDRFs.American journal of physiology. Heart and circulatory physiology · 2012Article
- Endothelium-derived hyperpolarizing factor and diabetes.World journal of cardiology · 2011Article
- 3',4'-Dihydroxyflavonol reduces superoxide and improves nitric oxide function in diabetic rat mesenteric arteries.PloS one · 2011Article
- Plasminogen activator inhibitor-1 regulates myoendothelial junction formation.Circulation research · 2010Article
- Endothelial Ca+-activated K+ channels in normal and impaired EDHF-dilator responses--relevance to cardiovascular pathologies and drug discovery.British journal of pharmacology · 2009Review
- The myoendothelial junction: breaking through the matrix?Microcirculation (New York, N.Y. : 1994) · 2009Review
- Role of EDHF in type 2 diabetes-induced endothelial dysfunction.American journal of physiology. Heart and circulatory physiology · 2008Article
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3 authors.
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Abstract
Experiments were designed to investigate the mechanisms underlying the diabetes-related impairment of the vasodilatations of the perfused mesenteric arterial bed induced by acetylcholine (ACh) and K(+). In streptozotocin (STZ)-diabetic rats, the ACh-induced endothelium-dependent vasodilatation was attenuated. The dose-response curves for ACh in control and diabetic rats were each shifted to the right by N(G)-nitro-L-arginine (L-NOARG) and by isotonic high K(+) (60 mM). The ACh dose-response curves under isotonic high K(+) were not different between control and diabetic rats. We also examined the vasodilatation induced by K(+), which is a putative endothelium-derived hyperpolarizing factor (EDHF). The mesenteric vasodilatation induced by a single administration of K(+) was greatly impaired in STZ-induced diabetic rats. Treatment with charybdotoxin plus apamin abolished the ACh-induced vasodilatation but enhanced the K(+)-induced response in controls and diabetic rats. After pretreatment with ouabain plus BaCl(2), the ACh-induced vasodilatation was significantly impaired and the K(+)-induced relaxation was abolished in both control and diabetic rats. The impairment of the endothelium-dependent vasodilatation of the mesenteric arterial bed seen in STZ-induced diabetic rats may be largely due to a defective vascular response to EDHF. It is further suggested that K(+) is one of the endothelium-derived hyperpolarizing factors and that the vasodilatation response to K(+) is impaired in the mesenteric arterial bed from diabetic rats.
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