ArticleJournal of vascular research2010
Nitric oxide suppresses cerebral vasomotion by sGC-independent effects on ryanodine receptors and voltage-gated calcium channels.
Article in Journal of vascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Far-infrared therapy for cardiovascular, autoimmune, and other chronic health problems: A systematic review.Experimental biology and medicine (Maywood, N.J.) · 2015Pooled it
- Nitric oxide is not responsible for initial sensory-induced neurovascular coupling response in the barrel cortex of lightly anesthetized mice.Neurophotonics · 2025Article
- Spreading depolarizations pose critical energy challenges in acute brain injury.Journal of neurochemistry · 2024Review
- Endothelial Nitric Oxide Suppresses Action-Potential-Like Transient Spikes and Vasospasm in Small Resistance Arteries.Hypertension (Dallas, Tex. : 1979) · 2020Article
- 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
- Modulation of cardiac L-type Ca2+ current by angiotensin-(1-7): normal versus heart failure.Therapeutic advances in cardiovascular disease · 2015Article
- Membrane potential and Ca2+ concentration dependence on pressure and vasoactive agents in arterial smooth muscle: A model.The Journal of general physiology · 2015Article
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Is Vasomotion in Cerebral Arteries Impaired in Alzheimer's Disease?Journal of Alzheimer's disease : JAD · 2015Review
- Systems biology of HBOC-induced vasoconstriction.Current drug discovery technologies · 2012Review
- Effects of somatothermal far-infrared ray on primary dysmenorrhea: a pilot study.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- Article
- Learning on Jupiter, learning on the Moon: the dark side of the G-force. Effects of gravity changes on neurovascular unit and modulation of learning and memory.Frontiers in behavioral neuroscience · 2012Article
- Modeling Ca2+ signaling in the microcirculation: intercellular communication and vasoreactivity.Critical reviews in biomedical engineering · 2011Review
- Inhibition of hypoxic pulmonary vasoconstriction of rats by carbon monoxide.Journal of Korean medical science · 2010Article
- The promise of inhibition of smooth muscle tone as a treatment for erectile dysfunction: where are we now?International journal of impotence researchReview
- Evidence both L-type and non-L-type voltage-dependent calcium channels contribute to cerebral artery vasospasm following loss of NO in the rat.Vascular pharmacologyArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsIn cerebral arteries, nitric oxide (NO) release plays a key role in suppressing vasomotion. Our aim was to establish the pathways affected by NO in rat middle cerebral arteries.
methodsIn isolated segments of artery, isometric tension and simultaneous measurements of either smooth muscle membrane potential or intracellular [Ca(2+)] ([Ca(2+)](SMC)) changes were recorded.
resultsIn the absence of L-NAME, asynchronous propagating Ca(2+) waves were recorded that were sensitive to block with ryanodine, but not nifedipine. L-NAME stimulated pronounced vasomotion and synchronous Ca(2+) oscillations with close temporal coupling between membrane potential, tone and [Ca(2+)](SMC). If nifedipine was applied together with L-NAME, [Ca(2+)](SMC) decreased and synchronous Ca(2+) oscillations were lost, but asynchronous propagating Ca(2+) waves persisted. Vasomotion was similarly evoked by either iberiotoxin, or by ryanodine, and to a lesser extent by ODQ. Exogenous application of NONOate stimulated endothelium-independent hyperpolarization and relaxation of either L-NAME-induced or spontaneous arterial tone. NO-evoked hyperpolarization involved activation of BK(Ca) channels via ryanodine receptors (RYRs), with little involvement of sGC. Further, in whole cell mode, NO inhibited current through L-type voltage-gated Ca(2+) channels (VGCC), which was independent of both voltage and sGC.
conclusionNO exerts sGC-independent actions at RYRs and at VGCC, both of which normally suppress cerebral artery myogenic tone.
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Registered trials
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