ArticleBritish journal of pharmacology2000
Stimulus-specific alteration of the relationship between cytosolic Ca(2+) transients and nitric oxide production in endothelial cells ex vivo.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 40 citations in OpenAlex.
- Apelin/APJ signaling in IGF-1-induced acute mitochondrial and antioxidant effects in spontaneously hypertensive rat myocardium.Journal of physiology and biochemistry · 2024Article
- Can endothelial hemoglobin-α regulate nitric oxide vasodilatory signaling?American journal of physiology. Heart and circulatory physiology · 2017Article
- Plasma kallikrein promotes epidermal growth factor receptor transactivation and signaling in vascular smooth muscle through direct activation of protease-activated receptors.The Journal of biological chemistry · 2010Article
- A mathematical model of vasoreactivity in rat mesenteric arterioles. II. Conducted vasoreactivity.American journal of physiology. Heart and circulatory physiology · 2010Article
- A mathematical model of vasoreactivity in rat mesenteric arterioles: I. Myoendothelial communication.Microcirculation (New York, N.Y. : 1994) · 2009Article
- Endothelial function in aorta segments of apolipoprotein E-deficient mice before development of atherosclerotic lesions.Pflugers Archiv : European journal of physiology · 2008Article
- The influence of statins on the free intracellular calcium concentration in human umbilical vein endothelial cells.BMC cardiovascular disorders · 2004Article
- Capacitative Ca(2+) entry in vascular endothelial cells is mediated via pathways sensitive to 2 aminoethoxydiphenyl borate and xestospongin C.British journal of pharmacology · 2002Article
- Mechanisms of the thapsigargin-induced Ca(2+) entry in in situ endothelial cells of the porcine aortic valve and the endothelium-dependent relaxation in the porcine coronary artery.British journal of pharmacology · 2000Article
- In vitro surfactant mitigation of gas bubble contact-induced endothelial cell death.Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, IncArticle
- Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts.Journal of pharmacology & pharmacotherapeuticsArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. To investigate the quantitative relationship between elevation in the intracellular Ca(2+) concentration ([Ca(2+)](i)) and nitric oxide (NO) production, the changes in [Ca(2+)](i) and NO production were determined in parallel, using fluorimetry of fura-2 and 2, 3-diaminonaphthalene, respectively, in endothelial cells ex vivo of pig aortic valves. 2. The extent of [Ca(2+)](i) elevation was quantitatively assessed by two parameters: the level of peak [Ca(2+)](i) elevation and the area under the [Ca(2+)](i) curve during treatment (the integrated [Ca(2+)](i) elevation). The amount of NO production was expressed as a percentage of that obtained with 10 microM ATP for 3 min. 3. ATP, bradykinin, thrombin, and ionomycin were used as stimulation to induce NO production, and all these caused [Ca(2+)](i) increases and NO production in a concentration-dependent manner. 4. The relationships between the peak [Ca(2+)](i) and NO production or between the integrated [Ca(2+)](i) elevation and NO production were well described by a straight line. However, the slope value of the linear relationship in both cases varied with the type of stimulation, with thrombin giving the greatest value, followed by ATP, bradykinin and ionomycin. 5. These data suggest that in endothelial cells ex vivo: (1) [Ca(2+)](i) elevation regulates NO production, but (2) the peak [Ca(2+)](i) elevation- or the integrated [Ca(2+)](i) elevation-NO production relationships varies depending on the type of agonists. Our results thus demonstrate the presence of the agonists-dependent modulation of the relationship between [Ca(2+)](i) elevation and NO production in endothelial cells ex vivo.
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