ArticleThe Journal of physiology1995
Apamin-sensitive K+ channels mediate an endothelium-dependent hyperpolarization in rabbit mesenteric arteries.
Article in The Journal of physiology, 1995. 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, 169 citations in OpenAlex.
- Mechanisms underlying selective coupling of endothelial CaThe Journal of physiology · 2020Article
- The triterpenoid alpha, beta-amyrin prevents the impaired aortic vascular reactivity in high-fat diet-induced obese mice.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Endothelial-derived hyperpolarization contributes to acetylcholine-mediated vasodilation in human skin in a dose-dependent manner.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Article
- Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction--a novel mechanism for maintaining vascular function.Journal of hematology & oncology · 2014Review
- Decoding dynamic Ca(2+) signaling in the vascular endothelium.Frontiers in physiology · 2014Article
- Article
- Dynamic Ca(2+) signal modalities in the vascular endothelium.Microcirculation (New York, N.Y. : 1994) · 2012Review
- Connexins and gap junctions in the EDHF phenomenon and conducted vasomotor responses.Pflugers Archiv : European journal of physiology · 2010Review
- Endothelium-derived hyperpolarising factors and associated pathways: a synopsis.Pflugers Archiv : European journal of physiology · 2010Review
- Upregulation of intermediate calcium-activated potassium channels counterbalance the impaired endothelium-dependent vasodilation in stroke-prone spontaneously hypertensive rats.Translational research : the journal of laboratory and clinical medicine · 2009Article
- Possible Involvement of Ca Activated K Channels, SK Channel, in the Quercetin-Induced Vasodilatation.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2009Article
- Role of arachidonic acid lipoxygenase metabolites in the regulation of vascular tone.American journal of physiology. Heart and circulatory physiology · 2009Review
- Potassium channels in the regulation of pulmonary artery smooth muscle cell proliferation and apoptosis: pharmacotherapeutic implications.British journal of pharmacology · 2008Review
- Role of SK(Ca) and IK(Ca) in endothelium-dependent hyperpolarizations of the guinea-pig isolated carotid artery.British journal of pharmacology · 2005Article
- The endothelium in health and disease: A discussion of the contribution of non-nitric oxide endothelium-derived vasoactive mediators to vascular homeostasis in normal vessels and in type II diabetes.Molecular and cellular biochemistry · 2004Article
- Small and intermediate conductance Ca(2+)-activated K+ channels confer distinctive patterns of distribution in human tissues and differential cellular localisation in the colon and corpus cavernosum.Naunyn-Schmiedeberg's archives of pharmacology · 2004Article
- Endothelium-dependent smooth muscle hyperpolarization: do gap junctions provide a unifying hypothesis?British journal of pharmacology · 2004Review
- Small- and intermediate-conductance calcium-activated K+ channels provide different facets of endothelium-dependent hyperpolarization in rat mesenteric artery.The Journal of physiology · 2003Article
- Involvement of H2O2 in superoxide-dismutase-induced enhancement of endothelium-dependent relaxation in rabbit mesenteric resistance artery.British journal of pharmacology · 2003Article
- Apamin inhibits NO-induced relaxation of the spontaneous contractile activity of the myometrium from non-pregnant women.Reproductive biology and endocrinology : RB&E · 2003Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
1. Vascular endothelial cells release a variety of substances which affect the membrane potential and tone of underlying vascular smooth muscle. In the presence of N omega-nitro-L-arginine to inhibit nitric oxide synthase and indomethacin to inhibit cyclo-oxygenase, acetylcholine (ACh; EC50 approximately 1 microM) elicited the release of an endothelium-derived hyperpolarizing factor (EDHF) in rabbit mesenteric arteries. 2. The hyperpolarization due to EDHF was blocked by apamin (IC50 approximately 0.3 nM), and by other inhibitors of the apamin-sensitive K+ channel (10 nM scyllatoxin, 100 microM d-tubocurarine, 300 microM gallamine) in the presence of indomethacin and N omega-nitro-L-arginine. The hyperpolarization was not blocked by glibenclamide (5 microM), iberiotoxin (10 nM), tetraethylammonium (1 mM), barium (500 microM), 4-aminopyridine (500 microM), ouabain (10 microM), bumetanide (10 microM), or nimodipine (100 nM). 3. In the presence of apamin and N omega-nitro-L-arginine, but the absence of indomethacin, ACh triggered a hyperpolarization that was blocked by glibenclamide, an inhibitor of ATP-sensitive K+ (KATP) channels. A similar glibenclamide-sensitive hyperpolarization was caused by Iloprost, a stable analogue of prostacyclin. 4. In experiments which distinguished the effects of EDHF, prostanoids and nitric oxide, hyperpolarizations and/or relaxations triggered by ACh were antagonized by muscarinic antagonists, the relative potencies (atropine approximately 4-DAMP > pirenzepine) of which indicated that the release of all three endothelium-derived factors was mediated by M3 receptors. 5. Our results suggest that ACh stimulates M3 receptors on endothelial cells, triggering the release of nitric oxide and prostanoids, which hyperpolarize underlying smooth muscle by activation of KATP channels, and the release of an EDHF, which hyperpolarizes smooth muscle through the activation of apamin-sensitive K+ (KAS) channels.
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