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

Journal article
Authors Awahan Rahman
Alun Hughes
Vladimir Matchkov
Holger Nilsson
Christian Aalkjaer
Published in Cell calcium
Volume 42
Issue 6
Pages 536-47
ISSN 0143-4160
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages 536-47
Language en
Links dx.doi.org/10.1016/j.ceca.2007.01.0...
Keywords Animals, Apamin, pharmacology, Calcium, metabolism, Calcium Signaling, drug effects, Charybdotoxin, pharmacology, Endothelial Cells, cytology, drug effects, physiology, Endothelium, Vascular, cytology, drug effects, physiology, Indoles, pharmacology, Indomethacin, pharmacology, Male, Membrane Potentials, drug effects, Mesenteric Arteries, drug effects, metabolism, physiology, Microscopy, Confocal, Models, Biological, Muscle, Smooth, drug effects, metabolism, physiology, NG-Nitroarginine Methyl Ester, pharmacology, Nifedipine, pharmacology, Norepinephrine, pharmacology, Potassium, metabolism, Rats, Rats, Wistar, Ryanodine, pharmacology, Vasomotor System, cytology, drug effects, physiology
Subject categories Medical and Health Sciences

Abstract

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 1 min(-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 40 mM 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 [Ca2+]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 [Ca2+]i in the two cell types.

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