ArticleThe Journal of physiology2002
Nitric oxide inhibits capacitative Ca2+ entry and enhances endoplasmic reticulum Ca2+ uptake in bovine vascular endothelial cells.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 135 citations in OpenAlex.
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- The Emerging Role of Endothelial Ion Channels in the Control of Human Microcirculation.International journal of molecular sciences · 2026Review
- The machinery of healthy vasoconstriction: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- Cell-specific copper dyshomeostasis mechanism in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Lipid Emulsions Inhibit Labetalol-Induced Vasodilation in the Isolated Rat Aorta.International journal of molecular sciences · 2024Article
- Cracking the Endothelial Calcium (CaInternational journal of molecular sciences · 2023Review
- The Molecular Heterogeneity of Store-Operated CaInternational journal of molecular sciences · 2023Review
- Characterization of endothelium-dependent and -independent processes in occipital artery of the rat: relevance to control of blood flow to nodose sensory cells.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Cyclopiazonic Acid-Induced CaFrontiers in physiology · 2021Article
- Resveratrol inhibits CaEnvironmental health and preventive medicine · 2020Article
- Review
- The Role of Endothelial CaInternational journal of molecular sciences · 2018Review
- Endothelial CaInternational journal of molecular sciences · 2018Review
- Cholesterol Enrichment Impairs Capacitative Calcium Entry, eNOS Phosphorylation & Shear Stress-Induced NO Production.Cellular and molecular bioengineering · 2017Article
- Shear stress-induced NO production is dependent on ATP autocrine signaling and capacitative calcium entry.Cellular and molecular bioengineering · 2014Article
- Article
- Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters.World journal of biological chemistry · 2012Article
- cGMP reduces the sarcoplasmic reticulum Ca2+ loading in airway smooth muscle cells: a putative mechanism in the regulation of Ca2+ by cGMP.Journal of muscle research and cell motility · 2012Article
- TRP channels: sensors and transducers of gasotransmitter signals.Frontiers in physiology · 2012Article
- P2Y receptors as regulators of lung endothelial barrier integrity.Journal of cardiovascular disease research · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In vascular endothelial cells, elevation of cytosolic free calcium concentration ([Ca2+]i) causes activation of nitric oxide synthase (NOS) and release of nitric oxide (NO). The goal of the study was to characterize the interplay between [Ca2+]i and NO production in this cell type. Simultaneous measurements of [Ca2+]i and intracellular NO concentration ([NO]i) in cultured bovine vascular endothelial cells (CPAE cell line) with the fluorescent indicators fura-2 and DAF-2, respectively, revealed that Ca2+ influx following agonist-induced intracellular Ca2+ store depletion (capacitative Ca2+ entry, CCE) represents the preferential Ca2+ source for the activation of the Ca2+-calmodulin-dependent endothelial NOS (eNOS). Exposure to the NO donor sodium nitroprusside (SNP) showed that high NO levels suppressed CCE and had an inhibitory effect on Ca2+ extrusion by the plasmalemmal Ca2+-ATPase. This inhibitory effect on CCE was mimicked by the membrane-permeant cGMP analogue 8-bromo-cGMP, but was reversed by the NO scavenger haemoglobin and prevented by the inhibitor of the NO-sensitive guanylate cyclase ODQ. Brief exposure to SNP reduced the peak of ATP-induced Ca2+ release from the endoplasmic reticulum (ER) and accelerated Ca2+ reuptake into the ER. Prolonged incubation with SNP resulted in enhanced Ca2+ loading of the ER, as revealed by direct measurements of store content with the ER-entrapped low-affinity Ca2+ indicator mag-fura-2. The results suggest that in vascular endothelial cells, NO synthesis is under autoregulatory control that involves NO-dependent [Ca2+]i regulation. Via cGMP-dependent inhibition of CCE and acceleration of Ca2+ sequestration into the ER, NO can lower [Ca2+]i and therefore exert an autoregulatory negative feedback on its own Ca2+-dependent synthesis.
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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.