ArticleBritish journal of pharmacology2010
Impairment of endothelial SK(Ca) channels and of downstream hyperpolarizing pathways in mesenteric arteries from spontaneously hypertensive rats.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 74 citations in OpenAlex.
- Cerebral capillary computation.American journal of physiology. Cell physiology · 2026Review
- The machinery of healthy vasodilatation: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- CaInternational journal of molecular sciences · 2023Review
- Endothelial Nitric Oxide Suppresses Action-Potential-Like Transient Spikes and Vasospasm in Small Resistance Arteries.Hypertension (Dallas, Tex. : 1979) · 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
- Modulation of Cardiovascular Function in Primary Hypertension in Rat by SKA-31, an Activator ofInternational journal of molecular sciences · 2019Article
- Pharmacological Targeting of KCa Channels to Improve Endothelial Function in the Spontaneously Hypertensive Rat.International journal of molecular sciences · 2019Article
- Gain-of-Function Mutations in KCNN3 Encoding the Small-Conductance CaAmerican journal of human genetics · 2019Article
- Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels.International journal of molecular sciences · 2018Review
- Hyperandrogenemia reduces endothelium-derived hyperpolarizing factor-mediated relaxation in mesenteric artery of female rats.Biology of reproduction · 2017Article
- KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Inward rectifier potassium (Kir2.1) channels as end-stage boosters of endothelium-dependent vasodilators.The Journal of physiology · 2016Article
- Genetic deficit of KBritish journal of pharmacology · 2015Article
- Enalapril Normalizes Endothelium-Derived Hyperpolarizing Factor-Mediated Relaxation in Mesenteric Artery of Adult Hypertensive Rats Prenatally Exposed to Testosterone.Biology of reproduction · 2015Article
- Reduced activity of SKC a and Na-K ATPase underlies the accelerated impairment of EDH-type relaxations in mesenteric arteries of aging spontaneously hypertensive rats.Pharmacology research & perspectives · 2015Article
- Vascular inward rectifier K+ channels as external K+ sensors in the control of cerebral blood flow.Microcirculation (New York, N.Y. : 1994) · 2015Review
- 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
- Extracellular Calcium-Dependent Modulation of Endothelium Relaxation in Rat Mesenteric Small Artery: The Role of Potassium Signaling.BioMed research international · 2015Article
- AKAP150-dependent cooperative TRPV4 channel gating is central to endothelium-dependent vasodilation and is disrupted in hypertension.Science signaling · 2014Article
- Targeting the Small- and Intermediate-Conductance Ca-Activated Potassium Channels: The Drug-Binding Pocket at the Channel/Calmodulin Interface.Neuro-Signals · 2014Review
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4 authors at 1 institution in 1 country.
Funding
Abstract
background and purposePrevious studies have shown that endothelium-dependent hyperpolarization of myocytes is reduced in resistance arteries from spontaneously hypertensive rats (SHRs). The aim of the present study was to determine whether this reflects down-regulation of endothelial K(+) channels or their associated pathways. EXPERIMENTAL APPROACH: Changes in vascular K(+) channel responses and expression were determined by a combination of membrane potential recordings and Western blotting. KEY
resultsEndothelium-dependent myocyte hyperpolarizations induced by acetylcholine, 6,7-dichloro-1H-indole-2,3-dione 3-oxime (NS309) (opens small- and intermediate-conductance calcium-sensitive K(+) channels, SK(Ca) and IK(Ca), respectively) or cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (SK(Ca) opener) were reduced in mesenteric arteries from SHRs. After blocking SK(Ca) channels with apamin, hyperpolarizations to acetylcholine and NS309 in SHR arteries were similar to those of controls. Hyperpolarization to 5 mM KCl was reduced in SHR arteries due to loss of the Ba(2+)-sensitive, inward-rectifier channel (K(IR)) component; the contribution of ouabain-sensitive, Na(+)/K(+)-ATPases was unaffected. Protein expression of both SK(Ca) and K(IR) channels was reduced in SHR arteries; the caveolin-1 monomer/dimer ratio was increased. CONCLUSIONS AND IMPLICATIONS: In SHRs, the distinct pathway that generates endothelium-dependent hyperpolarization in vascular myocyte by activation of IK(Ca) channels and Na(+)/K(+)-ATPases remains intact. The second pathway, initiated by endothelial SK(Ca) channel activation and amplified by K(IR) opening on both endothelial cells and myocytes is compromised in SHRs due to down-regulation of both SK(Ca) and K(IR) and to changes in caveolin-1 oligomers. These impairments in the SK(Ca)-K(IR) pathway shed new light on vascular control mechanisms and on the underlying vascular changes in hypertension.
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