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

Adam Kapela, Anastasios Bezerianos, Nikolaos M. Tsoukias

Research output: Contribution to journalArticlepeer-review

Abstract

To study the effect of myoendothelial communication on vascular reactivity, we integrated detailed mathematical models of Ca2+ dynamics and membrane electrophysiology in arteriolar smooth muscle (SMC) and endothelial (EC) cells. Cells are coupled through the exchange of Ca2+, Cl-, K+, and Na1 ions, inositol 1,4,5-triphosphate (IP3), and the paracrine diffusion of nitric oxide (NO). EC stimulation reduces intracellular Ca2+ ([Ca2+]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 SKCa and IKCa channels. During NE stimulation, IP3 diffusing from the SMC induces EC Ca2+ release, which, in turn, moderates SMC depolarization and [Ca2+]i elevation. On the contrary, SMC [Ca2+]i was not affected by EC-derived IP3. Myoendothelial Ca2+ fluxes had no effect in either cell. The EC exerts a stabilizing effect on calcium-induced calcium release-dependent SMC Ca2+ 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.

Original languageEnglish (US)
Pages (from-to)694-713
Number of pages20
JournalMICROCIRCULATION
Volume16
Issue number8
DOIs
StatePublished - Nov 2009

Keywords

  • Calcium dynamics
  • Computer simulations
  • EDHF
  • Gap junctions
  • Nitric oxide

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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