ArticleJournal of the American Heart Association2018
The Unexpected Role of Calcium-Activated Potassium Channels: Limitation of NO-Induced Arterial Relaxation.
Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 36 citations in OpenAlex.
- Influence of Soluble Guanylate Cyclase on Cardiac, Vascular, and Renal Structure and Function: A Physiopathological Insight.International journal of molecular sciences · 2025Review
- Sexually dimorphic mechanisms of HJournal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Potassium channel-mediated NO-induced vasodilation during maturation: Dominance of Kv7 channels.FASEB bioAdvances · 2025Article
- Dual role of calcium-activated potassium channels of high conductance: facilitator or limiter of NO-induced arterial relaxation?Frontiers in physiology · 2025Article
- Exercise training rescues impaired HAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- Myography of isolated blood vessels: Considerations for experimental design and combination with supplementary techniques.Frontiers in physiology · 2023Review
- The Effects of Acidosis on eNOS in the Systemic Vasculature: A Focus on Early Postnatal Ontogenesis.International journal of molecular sciences · 2022Review
- Sodium Nitroprusside-Induced Activation of Vascular Smooth Muscle BK Channels Is Mediated by PKG Rather Than by a Direct Interaction with NO.International journal of molecular sciences · 2022Article
- Preeclampsia: Linking Placental Ischemia with Maternal Endothelial and Vascular Dysfunction.Comprehensive Physiology · 2020Article
- Integrated analysis of lncRNAs and mRNAs reveals key trans-target genes associated with ETEC-F4ac adhesion phenotype in porcine small intestine epithelial cells.BMC genomics · 2020Article
- The Functional Availability of Arterial Kv7 Channels Is Suppressed Considerably by Large-Conductance Calcium-Activated Potassium Channels in 2- to 3-Month Old but Not in 10- to 15-Day Old Rats.Frontiers in physiology · 2020Article
- Article
- The Unexpected Role of Calcium-Activated Potassium Channels: Limitation of NO-Induced Arterial Relaxation.Journal of the American Heart Association · 2018Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMultiple studies have shown that an NO-induced activation of vascular smooth muscle BK channels contributes to the NO-evoked dilation in many blood vessels. In vivo, NO is released continuously. NO attenuates vessel constrictions and, therefore, exerts an anticontractile effect. It is unknown whether the anticontractile effect of continuously present NO is mediated by BK channels. METHODS AND
resultsThis study tested the hypothesis that BK channels mediate the vasodilatory effect of continuously present NO. Experiments were performed on rat and mouse tail and rat saphenous arteries using isometric myography and FURA-2 fluorimetry. Continuously present NO donors, as well as endogenous NO, attenuated methoxamine-induced vasoconstrictions. This effect was augmented in the presence of the BK channel blocker iberiotoxin. Moreover, the contractile effect of iberiotoxin was reduced in the presence of NO donors. The effect of the NO donor sodium nitroprusside was abolished by an NO scavenger and by a guanylyl cyclase inhibitor. In addition, the effect of sodium nitroprusside was reduced considerably by a protein kinase G inhibitor, but was not altered by inhibition of H
conclusionsIn summary, this study demonstrates the following: (1) continuously present NO evokes a strong anticontractile effect on rat and mouse arteries; (2) the iberiotoxin-induced augmentation of the effect of NO is associated with an NO-induced reduction of the effect of iberiotoxin; and (3) NO evoked a reduction of calcium influx via L-type calcium channels.
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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.