ArticleBritish journal of pharmacology2001
Cellular target of voltage and calcium-dependent K(+) channel blockers involved in EDHF-mediated responses in rat superior mesenteric artery.
Article in British journal of pharmacology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 51 citations in OpenAlex.
- Acetylcholine activates a regenerative vasodilator mechanism that is sensitive to nitric oxide production.Frontiers in physiology · 2025Article
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- Braylin induces a potent vasorelaxation, involving distinct mechanisms in superior mesenteric and iliac arteries of rats.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
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- Novel role of endothelial BKCa channels in altered vasoreactivity following hypoxia.American journal of physiology. Heart and circulatory physiology · 2010Article
- Connexins and gap junctions in the EDHF phenomenon and conducted vasomotor responses.Pflugers Archiv : European journal of physiology · 2010Review
- NS309 restores EDHF-type relaxation in mesenteric small arteries from type 2 diabetic ZDF rats.British journal of pharmacology · 2010Article
- Hypercholesterolemia suppresses Kir channels in porcine bone marrow progenitor cells in vivo.Biochemical and biophysical research communications · 2007Article
- Combination of Ca2+ -activated K+ channel blockers inhibits acetylcholine-evoked nitric oxide release in rat superior mesenteric artery.British journal of pharmacology · 2006Article
- Membrane hyperpolarization is not required for sustained muscarinic agonist-induced increases in intracellular Ca2+ in arteriolar endothelial cells.Microcirculation (New York, N.Y. : 1994) · 2005Article
- Spreading dilatation in rat mesenteric arteries associated with calcium-independent endothelial cell hyperpolarization.The Journal of physiology · 2004Article
- Endothelium-dependent smooth muscle hyperpolarization: do gap junctions provide a unifying hypothesis?British journal of pharmacology · 2004Review
- Inhibition of EDHF by two new combinations of K+-channel inhibitors in rat isolated mesenteric arteries.British journal of pharmacology · 2003Article
- Smooth muscle membrane potential modulates endothelium-dependent relaxation of rat basilar artery via myo-endothelial gap junctions.The Journal of physiology · 2002Article
- Characterization of a charybdotoxin-sensitive intermediate conductance Ca2+-activated K+ channel in porcine coronary endothelium: relevance to EDHF.British journal of pharmacology · 2002Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We have investigated the cellular target of K(+) channel blockers responsible for the inhibition of the EDHF-mediated relaxation in the rat mesenteric artery by studying their effects on tension, smooth muscle cell (SMC) membrane potential and endothelial cell Ca(2+) signal ([Ca(2+)](endo)). 2. In arteries contracted with prostaglandin F(2 alpha) (2.5 - 10 microM), relaxation evoked by ACh (0.01 - 3 microM) was abolished by a combination of charybdotoxin (ChTX, 0.1 microM) plus apamin (Apa, 0.1 microM) and was inhibited by 68+/-6% (n=6) by 4-aminopyridine (4-AP, 5 mM). 3. ACh(0.001 - 3 microM) increased [Ca(2+)](endo) and hyperpolarized SMCs with the same potency, the pD(2) values were equal to 7.2+/-0.08 (n=4) and 7.2+/-0.07 (n=9), respectively. SMCs hyperpolarization to ACh (1 microM) was abolished by high K(+) solution or by ChTX/Apa. It was decreased by 66+/-5% (n=6) by 4-AP. 4. The increase in [Ca(2+)](endo) evoked by ACh (1 microM) was insensitive to ChTX/Apa but was depressed by 58+/-16% (n=6) and 27+/-4% (n=7) by raising external K(+) concentration and by 4-AP, respectively. 5. The effect of 4-AP on [Ca(2+)](endo) was not affected by increasing external K(+) concentration. In Ca-free/EGTA solution, the transient increase in [Ca(2+)](endo) evoked by ACh (1 microM) was abolished by thapsigargin (1 microM) and was decreased by 75+/-7% (n=5) by 4-AP. 6. These results show that inhibition of EDHF-evoked responses by 4-AP may be attributed to a decrease in the Ca(2+) release activated by ACh in endothelial cells. The abolition of SMCs hyperpolarization to ACh by ChTX/Apa is not related to an interaction with the [Ca(2+)](endo).
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