ArticleThe Journal of physiology2003
Small- and intermediate-conductance calcium-activated K+ channels provide different facets of endothelium-dependent hyperpolarization in rat mesenteric artery.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 186 citations in OpenAlex.
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- Effects of SGLT2 inhibitors on ion channels in heart failure: focus on the endothelium.Basic research in cardiology · 2025Review
- Acetylcholine activates a regenerative vasodilator mechanism that is sensitive to nitric oxide production.Frontiers in physiology · 2025Article
- Flow-Dependent Modulation of Endothelial CaBiomedicines · 2024Article
- Time-Dependent Relationship Between Endothelial Dysfunction and High Blood Pressure in Fructose Drinking Rats.Turkish journal of pharmaceutical sciences · 2024Article
- Potentiation of BKCa channels by cystic fibrosis transmembrane conductance regulator correctors VX-445 and VX-121.The Journal of clinical investigation · 2024Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- CaInternational journal of molecular sciences · 2023Review
- Cerebral arteriolar and neurovascular dysfunction after chemically induced menopause in mice.American journal of physiology. Heart and circulatory physiology · 2022Article
- Differential hyperpolarization to substance P and calcitonin gene-related peptide in smooth muscle versus endothelium of mouse mesenteric artery.Microcirculation (New York, N.Y. : 1994) · 2021Article
- Cyclopiazonic Acid-Induced CaFrontiers in physiology · 2021Article
- Calcium-Dependent Ion Channels and the Regulation of Arteriolar Myogenic Tone.Frontiers in physiology · 2021Review
- Polarized Proteins in Endothelium and Their Contribution to Function.Journal of vascular research · 2021Review
- Cytochrome P450 Epoxygenase-Dependent Activation of TRPV4 Channel Participates in Enhanced Serotonin-Induced Pulmonary Vasoconstriction in Chronic Hypoxic Pulmonary Hypertension.Analytical cellular pathology (Amsterdam) · 2020Article
- KFrontiers in physiology · 2020Article
- Role of KPflugers Archiv : European journal of physiology · 2019Article
- Adaptive reduction of human myometrium contractile activity in response to prolonged uterine stretch during term and twin pregnancy. Role of TREK-1 channel.Biochemical pharmacology · 2018Article
- Endothelium-Dependent Hyperpolarization (EDH) in Hypertension: The Role of Endothelial Ion Channels.International journal of molecular sciences · 2018Review
- Progesterone inhibits contraction and increases TREK-1 potassium channel expression in late pregnant rat uterus.Oncotarget · 2018Article
- Heteromeric TRPV4/TRPC1 channels mediate calcium-sensing receptor-induced nitric oxide production and vasorelaxation in rabbit mesenteric arteries.Vascular pharmacology · 2017Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of both small-conductance (SKCa) and intermediate-conductance (IKCa) Ca2+-activated K+ channels in endothelial cells leads to vascular smooth muscle hyperpolarization and relaxation in rat mesenteric arteries. The contribution that each endothelial K+ channel type makes to the smooth muscle hyperpolarization is unknown. In the presence of a nitric oxide (NO) synthase inhibitor, ACh evoked endothelium and concentration-dependent smooth muscle hyperpolarization, increasing the resting potential (approx. -53 mV) by around 20 mV at 3 microM. Similar hyperpolarization was evoked with cyclopiazonic acid (10 microM, an inhibitor of sarcoplasmic endoplasmic reticulum calcium ATPase (SERCA)) while 1-EBIO (300 microM, an IKCa activator) only increased the potential by a few millivolts. Hyperpolarization in response to either ACh or CPA was abolished with apamin (50 nM, an SKCa blocker) but was unaltered by 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (1 microM TRAM-34, an IKCa blocker). During depolarization and contraction in response to phenylephrine (PE), ACh still increased the membrane potential to around -70 mV, but with apamin present the membrane potential only increased just beyond the original resting potential (circa -58 mV). TRAM-34 alone did not affect hyperpolarization to ACh but, in combination with apamin, ACh-evoked hyperpolarization was completely abolished. These data suggest that true endothelium-dependent hyperpolarization of smooth muscle cells in response to ACh is attributable to SKCa channels, whereas IKCa channels play an important role during the ACh-mediated repolarization phase only observed following depolarization.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.