Vladimir Matchkov

Antiphase oscillations of endothelium and smooth muscle [Ca2+]i in vasomotion of rat mesenteric small arteries.

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  • Awahan Rahman, Denmark
  • Vladimir Matchkov
  • Alun Hughes, Department of Clinical Pharmacology, St. Mary's Hospital, University College London, United Kingdom
  • Holger Nilsson, Denmark
  • Christian Aalkjær
  • Danish Biomembrane Research Centre
The mechanisms leading to vasomotion in the presence of noradrenaline and inhibitors of the sarcoplasmic/endoplasmic reticulum calcium ATPase were investigated in isolated rat mesenteric small arteries. Isobaric diameter and isometric force were measured together with membrane potential in endothelial cells and smooth muscle cells (SMC). Calcium in the endothelial cells and SMC was imaged with confocal microscopy. In the presence of noradrenaline and cyclopiazonic acid, ryanodine-insensitive oscillations in tone were produced. The frequency was about 1min(-1) and amplitude about 70% of the maximal tone. The amplitude was reduced by indomethacin and increased with L-NAME. Vasomotion was inhibited by nifedipine and by 40mM potassium. The frequency was increased and amplitude decreased by removal of the endothelium and by application of charybdotoxin and apamin. The vasomotion was associated with in-phase oscillations of membrane potential in endothelial cells and SMC and oscillations of [Ca(2+)](i) that were in near anti-phase. We suggest a working model for the generation of oscillation based on a membrane oscillator where ion channels in both endothelial cells and SMC interact via a current running between the two cell types through myoendothelial gap junctions, which sets up a near anti-phase oscillation of [Ca(2+)](i) in the two cell types.
Original languageEnglish
JournalCell Calcium
Volume42
Issue6
Pages (from-to)536-547
Number of pages12
ISSN0143-4160
Publication statusPublished - 2007

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