ArticleThe Journal of physiology1995
Nitric oxide hyperpolarizes rabbit mesenteric arteries via ATP-sensitive potassium channels.
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 85 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
85 citing papers in PubMed, 357 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Unresolved mechanisms: a hypothesized spatial regulation of myosin light chain phosphorylation within the walls of resistance arteries.Frontiers in physiology · 2026Article
- Potassium channel-mediated NO-induced vasodilation during maturation: Dominance of Kv7 channels.FASEB bioAdvances · 2025Article
- Electro-metabolic signaling.The Journal of general physiology · 2024Article
- Unleashing the Potential of Nrf2: A Novel Therapeutic Target for Pulmonary Vascular Remodeling.Antioxidants (Basel, Switzerland) · 2023Review
- Kir6.1 and SUR2B in Cantú syndrome.American journal of physiology. Cell physiology · 2022Review
- ATP-Sensitive Potassium Channels in Migraine: Translational Findings and Therapeutic Potential.Cells · 2022Review
- The Use of Angiotensin II for the Treatment of Post-cardiopulmonary Bypass Vasoplegia.Cardiovascular drugs and therapy · 2022Review
- Omega-3 polyunsaturated fatty acid-induced vasodilation in mouse aorta and mesenteric arteries is not mediated by ATP-sensitive potassium channels.Frontiers in physiology · 2022Article
- The vital role for nitric oxide in intraocular pressure homeostasis.Progress in retinal and eye research · 2021Review
- Lipofundin MCT/LCT Inhibits Levcromakalim-Induced Vasodilation by Inhibiting Endothelial Nitric Oxide Release.International journal of molecular sciences · 2020Article
- Cardiac NaThe journal of physiological sciences : JPS · 2019Review
- Pinacidil, a KATP channel opener, stimulates cardiac NaNaunyn-Schmiedeberg's archives of pharmacology · 2019Article
- Article
- Ion Channels in Pulmonary Hypertension: A Therapeutic Interest?International journal of molecular sciences · 2018Review
- The Unexpected Role of Calcium-Activated Potassium Channels: Limitation of NO-Induced Arterial Relaxation.Journal of the American Heart Association · 2018Article
- Regulation of vascular tone homeostasis by NO and HBiochemical pharmacology · 2018Review
- The KThe journal of headache and pain · 2017Article
- Diazoxide protects rat vascular endothelial cells against hypoxia and cold-induced damage.Experimental and therapeutic medicine · 2017Article
- Vascular KRespiratory physiology & neurobiology · 2017Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
1. Nitric oxide (NO) relaxes vascular smooth muscle (VSM) by mechanisms which are not fully understood. One possibility is that NO hyperpolarizes membranes, thereby diminishing Ca2+ entry through voltage-dependent Ca2+ channels. In the current study, the effects of NO on membrane potential of rabbit mesenteric arteries were recorded using intracellular microelectrodes. 2. NO, released by 3-morpholinosydnonimine (SIN-1, 3 microM), reversibly hyperpolarized arteries by -9.5 +/- 4.0 mV (means +/- S.D., n = 97) from a resting membrane potential of -53.1 +/- 5.7 mV. The hyperpolarization was blocked by oxyhaemoglobin (20 microM), and only occurred in arteries pre-treated with N omega-nitro-L-arginine (100 microM) or denuded of endothelium. 3. The effect of SIN-1 was concentration dependent (EC50 approximately 0.4 microM) and its dose response was shifted to the left by zaprinast (100 microM), an inhibitor of cGMP-specific phosphodiesterases. 4. The hyperpolarization due to SIN-1 was modified by changes in extracellular K+ concentration, but not by changes in Ca2+, Na+ or Cl-. The hyperpolarization was blocked by glibenclamide (IC50 approximately 0.15 microM), but not by apamin (3-300 nM), barium (5-150 microM), tetraethylammonium (0.1-10 mM), or 4-aminopyridine (5-500 microM). The hyperpolarization due to lemakalim (0.03-3 microM), an activator of ATP-sensitive potassium channels (KATP), displayed the same sensitivities to these K+ channel blocking agents, whereas the endothelium-derived hyperpolarizing factor, triggered by the addition of acetylcholine (3 microM), caused a hyperpolarization (-15.3 +/- 6.2 mV) that was blocked by apamin, but not by any other agent. 5. These results suggest that NO hyperpolarizes VSM in rabbit mesenteric arteries by activating KATP channels, with the accumulation of cGMP as an intermediate step.
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