Reoxygenation-induced Ca2+ rise is mediated via Ca2+influx and Ca2+ release from the endoplasmic reticulum in cardiac endothelial cells

Conditions of ischemia-reperfusion disturb the homoeostasis of cytosolic Ca2+ in cardiac microvascular endothelial cells (CMEC), leading to numerous malfunctions of the endothelium. Reperfusion specifically aggravates the Ca2+ overload developed during sustained ischemia. The aim of this study was t...

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Veröffentlicht in:	Cardiovascular research 2007, Vol.73 (1), p.164-171
Hauptverfasser:	PETERS, Saskia C, PIPER, H. Michael
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biological and medical sciences Biological Transport Calcium - metabolism Cardiology. Vascular system Cell Hypoxia Cells, Cultured Cytosol - metabolism Endoplasmic Reticulum - metabolism Endothelial Cells - metabolism Guanidines - pharmacology Hydrogen-Ion Concentration Ion Channels - metabolism Male Medical sciences Microcirculation Myocardial Reperfusion Injury - metabolism Myocardium - metabolism Ouabain - pharmacology Rats Rats, Wistar Sarcoplasmic Reticulum Calcium-Transporting ATPases - antagonists & inhibitors Sodium - metabolism Sodium-Hydrogen Exchangers - antagonists & inhibitors Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors Sodium-Potassium-Exchanging ATPase - metabolism Sulfones - pharmacology Thapsigargin - pharmacology
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