ArticleThe Journal of physiology1999
Direct actions of nitric oxide on rat neurohypophysial K+ channels.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 91 citations in OpenAlex.
- Nitric Oxide Synthase Blockade Impairs Spontaneous Calcium Activity in Mouse Primary Hippocampal Culture Cells.International journal of molecular sciences · 2023Article
- Regulation of Ion Channel Function by Gas Molecules.Advances in experimental medicine and biology · 2021Review
- Gasotransmitter Heterocellular Signaling.Antioxidants & redox signaling · 2017Article
- Identification of Cav2-PKCβ and Cav2-NOS1 complexes as entities for ultrafast electrochemical coupling.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Nitric oxide stimulates matrix synthesis and deposition by adult human aortic smooth muscle cells within three-dimensional cocultures.Tissue engineering. Part A · 2015Article
- Development of nitric oxide synthase inhibitors for neurodegeneration and neuropathic pain.Chemical Society reviews · 2014Review
- Layer-specific modulation of neuronal excitability by 660-nm laser irradiation in mouse neocortex.Lasers in medical science · 2014Article
- Smooth muscle relaxation and activation of the large conductance Ca(++)-activated K+ (BK(Ca)) channel by novel oestrogens.British journal of pharmacology · 2013Article
- Nitric oxide potentiation of the homomeric ρ1 GABA(C) receptor function.British journal of pharmacology · 2012Article
- Activation of the cGMP/Protein Kinase G Pathway by Nitric Oxide Can Decrease TRPV1 Activity in Cultured Rat Dorsal Root Ganglion Neurons.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2012Article
- Nitric oxide donors enhance the frequency dependence of dopamine release in nucleus accumbens.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- Headache-type adverse effects of NO donors: vasodilation and beyond.British journal of pharmacology · 2010Review
- What is the real physiological NO concentration in vivo?Nitric oxide : biology and chemistry · 2009Review
- Modulation of BKCa channel gating by endogenous signaling molecules.Physiology (Bethesda, Md.) · 2009Review
- Vascular large conductance calcium-activated potassium channels: functional role and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2007Review
- Blockade of phosphodiesterase Type 5 enhances rat neurohypophysial excitability and electrically evoked oxytocin release.The Journal of physiology · 2007Article
- L-Arginine currents in rat cardiac ventricular myocytes.The Journal of physiology · 2007Article
- Effects of nitric oxide on expressions of nitrosocysteine and calcium-activated potassium channels in the supraoptic nuclei and neural lobe of dehydrated rats.Neuroscience letters · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. Nitric oxide (NO) has been shown to modulate neuropeptide secretion from the posterior pituitary. Here we show that NO activates large-conductance Ca2+-activated K+ (BK) channels in posterior pituitary nerve terminals. 2. NO, generated either by the photolysis of caged-NO or with chemical donors, irreversibly enhanced the component of whole-terminal K+ current due to BK channels and increased the activity of BK channels in excised patches. NO also inhibited the transient A-current. The time courses of these effects on K+ current were very different; activation of BK channels developed slowly over several minutes whereas inhibition of A-current immediately followed NO uncaging. 3. Activation of BK channels by NO occurred in the presence of guanylyl cyclase inhibitors and after removal of ATP or GTP from the pipette solution, suggesting a cGMP-independent signalling pathway. 4. The sulfhydryl alkylating agent N-ethyl maleimide (NEM) increased BK channel activity. Pretreatment with NEM occluded NO activation. 5. NO activation of BK channels occurred independently of voltage and cytoplasmic Ca2+ concentration. In addition, NO removed the strict Ca2+ requirement for channel activation, rendering channels highly active even at nanomolar Ca2+ levels. 6. These results suggest that NO, or a reactive nitrogen byproduct, chemically modifies nerve terminal BK channels or a closely associated protein and thereby produces an increase in channel activity. Such activation is likely to inhibit impulse activity in posterior pituitary nerve terminals and this may explain the inhibitory action of NO on secretion.
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Registered trials
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.