ArticleThe Journal of clinical investigation2002
Different mechanisms underlying the stimulation of K(Ca) channels by nitric oxide and carbon monoxide.
Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Gasotransmitter signaling in the brain: New frontiers for therapeutics.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Synergistic mitochondrial impairment by endogenously elevated cyanide and hydrogen sulfide in Down syndrome; commentary on: Cyanide overproduction impairs cellular bioenergetics in Down syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Regulation of the Cerebral Circulation During Development.Comprehensive Physiology · 2021Article
- Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD.Advances in experimental medicine and biology · 2021Article
- The role of TLR4 and HO-1 in neuroinflammation after subarachnoid hemorrhage.Journal of neuroscience research · 2020Review
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Carbon Monoxide Modulates Connexin Function through a Lipid Peroxidation-Dependent Process: A Hypothesis.Frontiers in physiology · 2016Article
- Carbon monoxide, hydrogen sulfide, and nitric oxide as signaling molecules in the gastrointestinal tract.Gastroenterology · 2014Review
- Pharmacological consequences of the coexpression of BK channel α and auxiliary β subunits.Frontiers in physiology · 2014Review
- Review article: carbon monoxide in gastrointestinal physiology and its potential in therapeutics.Alimentary pharmacology & therapeutics · 2013Review
- Cerebral artery signal transduction mechanisms: developmental changes in dynamics and Ca2+ sensitivity.Current vascular pharmacology · 2013Review
- Multifunctional role of astrocytes as gatekeepers of neuronal energy supply.Frontiers in cellular neuroscience · 2013Article
- Carbon Monoxide and the brain: time to rethink the dogma.Current pharmaceutical design · 2013Review
- Function and regulation of large conductance Ca(2+)-activated K+ channel in vascular smooth muscle cells.Drug discovery today · 2012Review
- Shared signaling pathways among gasotransmitters.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Carbon monoxide-activated Nrf2 pathway leads to protection against permanent focal cerebral ischemia.Stroke · 2011Article
- Identification of a novel bacterial K(+) channel.The Journal of membrane biology · 2011Article
- Carbon monoxide as an endogenous vascular modulator.American journal of physiology. Heart and circulatory physiology · 2011Review
- Heme oxygenase metabolites inhibit tubuloglomerular feedback in vivo.American journal of physiology. Heart and circulatory physiology · 2011Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms underlying the effects of nitric oxide (NO) and carbon monoxide (CO), individually and collectively, on large-conductance calcium-activated K(+) (K(Ca)) channels were investigated in rat vascular smooth muscle cells (SMCs). Both NO and CO increased the activity of native K(Ca) channels. Dehydrosoyasaponin-I, a specific agonist for beta subunit of K(Ca) channels, increased the open probability of native K(Ca) channels only when it was delivered to the cytoplasmic surface of membrane. CO, but not NO, further increased the activity of native K(Ca) channels that had been maximally stimulated by dehydrosoyasaponin-I. After treatment of SMCs with anti-K(Ca),beta subunit antisense oligodeoxynucleotides, the stimulatory effect of NO, but not of CO, on K(Ca) channels was nullified. CO, but not NO, enhanced the K(Ca) current densities of heterologously expressed cloned K(Ca),alpha subunit, showing that the presence of K(Ca),beta subunit is not a necessity for the effect of CO but essential for that of NO. Finally, pretreatment of SMCs with NO abolished the effects of subsequently applied CO or diethyl pyrocarbonate on K(Ca) channels. In summary, the stimulatory effects of CO and NO on K(Ca) channels rely on the specific interactions of these gases with K(Ca),alpha and K(Ca),beta subunits.
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