ArticleBritish journal of pharmacology1999
Levcromakalim causes indirect endothelial hyperpolarization via a myo-endothelial pathway.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 28 citations in OpenAlex.
- Endothelium-Derived Hyperpolarizing Factor and Myoendothelial Coupling: TheFrontiers in physiology · 2020Review
- Multiplicity of effectors of the cardioprotective agent, diazoxide.Pharmacology & therapeutics · 2013Review
- Inhibitory effects of glycyrrhetinic Acid on the delayed rectifier potassium current in Guinea pig ventricular myocytes and HERG channel.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Connexins and gap junctions in the EDHF phenomenon and conducted vasomotor responses.Pflugers Archiv : European journal of physiology · 2010Review
- Bradykinin-induced, endothelium-dependent responses in porcine coronary arteries: involvement of potassium channel activation and epoxyeicosatrienoic acids.British journal of pharmacology · 2005Article
- Junctional and nonjunctional effects of heptanol and glycyrrhetinic acid derivates in rat mesenteric small arteries.British journal of pharmacology · 2004Article
- Endothelium-dependent smooth muscle hyperpolarization: do gap junctions provide a unifying hypothesis?British journal of pharmacology · 2004Review
- Smooth muscle membrane potential modulates endothelium-dependent relaxation of rat basilar artery via myo-endothelial gap junctions.The Journal of physiology · 2002Article
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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
1. Effects of K+ channel opener, levcromakalim, on vascular endothelial cells were examined. Under voltage- and current-clamp conditions, application of acetylcholine to dispersed endothelial cells isolated from rabbit superior mesenteric artery (dispersed RMAECs) produced hyperpolarization and outward currents. On the other hand, dispersed RMAECs did not respond to levcromakalim. 2. When membrane potential was recorded from endothelium in a mesenteric arterial segment, exposure to levcromakalim in a concentration range of 0.1 to 3 microM caused concentration-dependent hyperpolarization. The hyperpolarization was observed in the absence of external Ca2+ and was inhibited by 10 microM glibenclamide. 3. The presence of 1 mM heptanol did not affect the levcromakalin-induced hyperpolarization, whereas treatment of the mesenteric arterial segment with 20 microM 18 beta-glycyrrhetinic acid significantly reduced the hyperpolarization. The response to acetylcholine of RMAECs in an arterial segment with 18 beta-glycyrrhetinic acid was, however, similar to that without 18 beta-glycyrrhetinic acid. 4. These suggest that although RMAECs themselves are functionally insensitive to levcromakalim, those in an arterial segment are hyperpolarized by levcromakalim via myo-endothelial electrical communication.
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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.