ArticleEuropean biophysics journal : EBJ2003
Modelling the electrophysiological endothelial cell response to bradykinin.
Article in European biophysics journal : EBJ, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Coronary Smooth Muscle Cell Calcium Dynamics: Effects of Bifurcation Angle on Atheroprone Conditions.Frontiers in physiology · 2018Article
- Role of microprojections in myoendothelial feedback--a theoretical study.The Journal of physiology · 2013Article
- Nitric oxide signaling in the microcirculation.Critical reviews in biomedical engineering · 2011Review
- Modeling Ca2+ signaling in the microcirculation: intercellular communication and vasoreactivity.Critical reviews in biomedical engineering · 2011Review
- A mathematical model of vasoreactivity in rat mesenteric arterioles: I. Myoendothelial communication.Microcirculation (New York, N.Y. : 1994) · 2009Article
- Role of the endothelium on arterial vasomotion.Biophysical journal · 2005Article
- Calcium dynamics and signaling in vascular regulation: computational models.Wiley interdisciplinary reviews. Systems biology and medicineReview
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
The goal of the present study is to construct a biophysical model of the coronary artery endothelial cell response to bradykinin. This model takes into account intracellular Ca2+ dynamics, membrane potential, a non-selective cation channel, and two Ca(2+)-dependent K+ channels, as well as intra- and extracellular Ca2+ sources. The model reproduces the experimental data available, and predicts certain quantities which would be hard to obtain experimentally, like the individual K+ channel currents when the membrane potential is allowed to freely evolve, the implication of epoxyeicosatrienoic acids (EETs), and the total K+ released during stimulation. The main results are: (1) the large-conductance K+ channel participates only very little in the overall response; (2) EETs are required in order to explain the experimental current-potential relationships, but are not an essential component of the bradykinin response; and (3) the total K+ released during stimulation gives rise to a concentration in the intercellular space which is of millimolar order. This concentration change is compatible with the hypothesis that K+ contributes to the endothelium-derived hyperpolarizing factor phenomenon.
Indexed as
Identifiers
12851795What OpenQuestion holds
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.