ArticleBritish journal of pharmacology2006
Impaired small-conductance Ca2+-activated K+ channel-dependent EDHF responses in Type II diabetic ZDF rats.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 72 citations in OpenAlex.
- Cerebral capillary computation.American journal of physiology. Cell physiology · 2026Review
- Role of Protein Kinase C in Metabolic Regulation of Coronary Endothelial Small Conductance Calcium-Activated Potassium Channels.Journal of the American Heart Association · 2024Article
- Chronic Inhibition of mROS Protects Against Coronary Endothelial Dysfunction in Mice With Diabetes.Frontiers in cell and developmental biology · 2021Article
- KCa channel activation normalizes endothelial function in Type 2 Diabetic resistance arteries by improving intracellular CaMetabolism: clinical and experimental · 2021Article
- Coronary endothelial dysfunction prevented by small-conductance calcium-activated potassium channel activator in mice and patients with diabetes.The Journal of thoracic and cardiovascular surgery · 2020Article
- Mesenteric arterial dysfunction in the UC Davis Type 2 Diabetes Mellitus rat model is dependent on pre-diabetic versus diabetic status and is sexually dimorphic.European journal of pharmacology · 2020Article
- Endothelium-Dependent Hyperpolarization (EDH) in Diabetes: Mechanistic Insights and Therapeutic Implications.International journal of molecular sciences · 2019Review
- Decreased coronary arteriolar response to KMolecular and cellular biochemistry · 2018Article
- Hyperglycaemia disrupts conducted vasodilation in the resistance vasculature of db/db mice.Vascular pharmacology · 2018Article
- The Protective Effect of Antioxidants Consumption on Diabetes and Vascular Complications.Diseases (Basel, Switzerland) · 2016Review
- Inactivation of Endothelial Small/Intermediate Conductance of Calcium-Activated Potassium Channels Contributes to Coronary Arteriolar Dysfunction in Diabetic Patients.Journal of the American Heart Association · 2015Article
- Impairment of IKCa channels contributes to uteroplacental endothelial dysfunction in rat diabetic pregnancy.American journal of physiology. Heart and circulatory physiology · 2015Article
- Preserved regulation of renal perfusion pressure by small and intermediate conductance KCa channels in hypertensive mice with or without renal failure.Pflugers Archiv : European journal of physiology · 2015Article
- Article
- Advanced glycation end products impair K(Ca)3.1- and K(Ca)2.3-mediated vasodilatation via oxidative stress in rat mesenteric arteries.Pflugers Archiv : European journal of physiology · 2014Article
- Endothelial arginine resynthesis contributes to the maintenance of vasomotor function in male diabetic mice.PloS one · 2014Article
- Article
- Low intrinsic exercise capacity in rats predisposes to age-dependent cardiac remodeling independent of macrovascular function.American journal of physiology. Heart and circulatory physiology · 2013Article
- KCa 3.1 channels maintain endothelium-dependent vasodilatation in isolated perfused kidneys of spontaneously hypertensive rats after chronic inhibition of NOS.British journal of pharmacology · 2012Article
- Diet-induced obesity impairs endothelium-derived hyperpolarization via altered potassium channel signaling mechanisms.PloS one · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have examined the relative contributions of small- and intermediate-conductance Ca(2+)-activated K(+) channels (SK(Ca) and IK(Ca)) to the endothelium-derived hyperpolarizing factor (EDHF) pathway response in small mesenteric arteries of Zucker Diabetic Fatty (ZDF) rats, before and after the development of Type II diabetes, together with Lean controls. Smooth muscle membrane potential was recorded using sharp microelectrodes in the presence of 10 microM indomethacin plus 100 microM N(omega)-nitro-L-arginine. SK(Ca) was selectively inhibited with 100 nM apamin, whereas IK(Ca) was blocked with 10 microM TRAM-39 (2-(2-chlorophenyl)-2,2-diphenylacetonitrile). Resting membrane potentials were similar in arteries from 17- to 20-week-old control and diabetic rats (approximately -54 mV). Responses elicited by 1 and 10 microM acetylcholine (ACh) were significantly smaller in the diabetic group (e.g. hyperpolarizations to -69.5 +/- 0.8 mV (ZDF; n = 12) and -73.2 +/- 0.6 mV (Lean; n = 12; P < 0.05) evoked by 10 microM ACh). The IK(Ca)-mediated components of the ACh responses were comparable between groups (hyperpolarizations to approximately -65 mV on exposure to 10 microM ACh). However, SK(Ca)-mediated responses were significantly reduced in the diabetic group (hyperpolarizations to -63.1 +/- 1.0 mV (ZDF; n = 6) and -71.5 +/- 1.2 mV (Lean; n = 6; P < 0.05) on exposure to 10 microM ACh. Impaired ACh responses were not observed in arteries from 5- to 6-week-old (pre-diabetic) animals. SK(Ca) subunit mRNA expression was increased in the diabetic group. The EDHF pathway, especially the SK(Ca)-mediated response, is impaired in Type II diabetic ZDF rats without a reduction in channel gene expression. These results may be particularly relevant to the microvascular complications of diabetes. The functional separation of SK(Ca) and IK(Ca) pathways is discussed.
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