Evidence map›Paper›PMID 19905969›Full record

ArticleMicrocirculation (New York, N.Y. : 1994)2009

A mathematical model of vasoreactivity in rat mesenteric arterioles: I. Myoendothelial communication.

Adam Kapela, Anastasios Bezerianos, Nikolaos M Tsoukias

Abstract read
In one paragraph

Article in Microcirculation (New York, N.Y. : 1994), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Can endothelial hemoglobin-α regulate nitric oxide vasodilatory signaling?American journal of physiology. Heart and circulatory physiology · 2017
    Article
  5. Review
  6. 3D time-varying simulations of CaInternational journal for numerical methods in biomedical engineering · 2017
    Article
  7. Origins of variation in conducted vasomotor responses.Pflugers Archiv : European journal of physiology · 2015
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Nitric oxide signaling in the microcirculation.Critical reviews in biomedical engineering · 2011
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Adam KapelaDepartment of Biomedical Engineering, Florida International University, Miami, Florida, USA.
Anastasios Bezerianos
Nikolaos M Tsoukias
Florida International University · USUniversity of Patras · GR

Funding

Theorectal and Experimental Investigations of Microcirculatory SignalingSC1HL095101 · NHLBI · FLORIDA INTERNATIONAL UNIVERSITY · PI TSOUKIAS, NIKOLAOS MICHAEL · 2008 to 2012
$1.4M
NHLBI NIH HHS SC1 HL095101NHLBI NIH HHS SC1HL095101
6 · The paper itself

Abstract

To study the effect of myoendothelial communication on vascular reactivity, we integrated detailed mathematical models of Ca(2+) dynamics and membrane electrophysiology in arteriolar smooth muscle (SMC) and endothelial (EC) cells. Cells are coupled through the exchange of Ca(2+), Cl(-), K(+), and Na(+) ions, inositol 1,4,5-triphosphate (IP(3)), and the paracrine diffusion of nitric oxide (NO). EC stimulation reduces intracellular Ca(2+) ([Ca(2+)](i)) in the SMC by transmitting a hyperpolarizing current carried primarily by K(+). The NO-independent endothelium-derived hyperpolarization was abolished in a synergistic-like manner by inhibition of EC SK(Ca) and IK(Ca) channels. During NE stimulation, IP(3) diffusing from the SMC induces EC Ca(2+) release, which, in turn, moderates SMC depolarization and [Ca(2+)](i) elevation. On the contrary, SMC [Ca(2+)](i) was not affected by EC-derived IP(3). Myoendothelial Ca(2+) fluxes had no effect in either cell. The EC exerts a stabilizing effect on calcium-induced calcium release-dependent SMC Ca(2+) oscillations by increasing the norepinephrine concentration window for oscillations. We conclude that a model based on independent data for subcellular components can capture major features of the integrated vessel behavior. This study provides a tissue-specific approach for analyzing complex signaling mechanisms in the vasculature.

Indexed as

Membrane PotentialsModels, TheoreticalAnimalsArteriolesCalciumCalcium SignalingElectrophysiologyEndothelial CellsInositol 1,4,5-TrisphosphateMuscle, Smooth, VascularMyocytes, Smooth MuscleNitric OxideNorepinephrineParacrine CommunicationRatsSplanchnic CirculationCalciumInositol 1,4,5-TrisphosphateNitric OxideNorepinephrine

Identifiers

PMID19905969
PMCPMC3547604
OpenAlexW2043697091

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.