ArticleThe Journal of physiology2009
De novo expression of Kv6.3 contributes to changes in vascular smooth muscle cell excitability in a hypertensive mice strain.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Renal TRPM3 Channels Regulate Blood Pressure via Tubuloglomerular Feedback and Plasma Volume Control.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Effects ofThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- The P2Y6 Receptor as a Potential Keystone in Essential Hypertension.Function (Oxford, England) · 2024Article
- Distinct potassium channel types in brain capillary pericytes.Biophysical journal · 2024Article
- Blockage of VEGF function by bevacizumab alleviates early-stage cerebrovascular dysfunction and improves cognitive function in a mouse model of Alzheimer's disease.Translational neurodegeneration · 2024Article
- Article
- Mechanism of use-dependent Kv2 channel inhibition by RY785.The Journal of general physiology · 2022Article
- Vascular smooth muscle ion channels in essential hypertension.Frontiers in physiology · 2022Review
- Ion channel molecular complexes in vascular smooth muscle.Frontiers in physiology · 2022Review
- Allisartan ameliorates vascular remodeling through regulation of voltage-gated potassium channels in hypertensive rats.BMC pharmacology & toxicology · 2021Article
- Kv1.3 Channel Inhibition Limits Uremia-Induced Calcification in Mouse and Human Vascular Smooth Muscle.Function (Oxford, England) · 2021Article
- Heteromeric KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- KMicrocirculation (New York, N.Y. : 1994) · 2018Review
- Regulation of voltage-gated potassium channels in vascular smooth muscle during hypertension and metabolic disorders.Microcirculation (New York, N.Y. : 1994) · 2018Review
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Differences in TRPC3 and TRPC6 channels assembly in mesenteric vascular smooth muscle cells in essential hypertension.The Journal of physiology · 2017Article
- Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth.Advances in pharmacology (San Diego, Calif.) · 2017Review
- The contribution of Kv2.2-mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons.Physiological reports · 2016Article
- Kv5, Kv6, Kv8, and Kv9 subunits: No simple silent bystanders.The Journal of general physiology · 2016Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Essential hypertension involves a gradual and sustained increase in total peripheral resistance, reflecting an increased vascular tone. This change associates with a depolarization of vascular myocytes, and relies on a change in the expression profile of voltage-dependent ion channels (mainly Ca(2+) and K(+) channels) that promotes arterial contraction. However, changes in expression and/or modulation of voltage-dependent K(+) channels (Kv channels) are poorly defined, due to their large molecular diversity and their vascular bed-specific expression. Here we endeavor to characterize the molecular and functional expression of Kv channels in vascular smooth muscle cells (VSMCs) and their regulation in essential hypertension, by using VSMCs from resistance (mesenteric) or conduit (aortic) arteries obtained from a hypertensive inbred mice strain, BPH, and the corresponding normotensive strain, BPN. Real-time PCR reveals a differential distribution of Kv channel subunits in the different vascular beds as well as arterial bed-specific changes under hypertension. In mesenteric arteries, the most conspicuous change was the de novo expression of Kv6.3 (Kcng3) mRNA in hypertensive animals. The functional relevance of this change was studied by using patch-clamp techniques. VSMCs from BPH arteries were more depolarized than BPN ones, and showed significantly larger capacitance values. Moreover, Kv current density in BPH VSMCs is decreased mainly due to the diminished contribution of the Kv2 component. The kinetic and pharmacological profile of Kv2 currents suggests that the expression of Kv6.3 could contribute to the natural development of hypertension.
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