Comparison of volatile anesthetic actions on intracellular calcium stores of vascular smooth muscle - Investigation in isolated systemic resistance arteries

Background: Volatile anesthetic actions on intracellular Ca2+ stores (i.e., sarcoplasmic reticulum [SR]) of vascular smooth muscle have not been fully elucidated. Methods: Using isometric force recording method and fura-2 fluorometry, the actions of four volatile anesthetics on SR were studied in isolated endothelium-denuded rat mesenteric arteries. Results: Halothane (greater than or equal to 3%) and enflurane (greater than or equal to 3%)t but not isoflurane and sevoflurane, increased the intracellular Ca2+ concentration ([Ca2+](i)) in Ca2+-free solution. These Ca2+-releasing actions were eliminated by procaine. When each anesthetic was applied during Ca2+ loading, halothane (greater than or equal to 3%) and enflurane (5%), but not isoflurane and sevoflurane, decreased the amount of Ca2+ in the SR. However, if halothane or enflurane was applied with procaine during Ca2+ loading, both anesthetics increased the amount of Ca2+ in the SR. The caffeine-induced increase in [Ca2+](i) was enhanced in the presence of halothane (greater than or equal to 1%), enflurane (greater than or equal to 1%), and isoflurane (greater than or equal to 3%) but was attenuated in the presence of sevoflurane (greater than or equal to 3%). The norepinephrine-induced increase in [Ca2+](i) was enhanced only in the presence of sevoflurane (greater than or equal to 3%). Not all of these anesthetic effects on the [Ca2+](i) were parallel with the simultaneously observed anesthetic effects on the force. Conclusions: In systemic resistance arteries, the halothane, enflurane, isoflurane, and sevoflurane differentially influence the SR functions. Both halothane and enflurane cause Ca2+ release from the caffeine-sensitive SR. In addition, both anesthetics appear to have a stimulating action on Ca2+ uptake in addition to the Ca2+-releasing action. Halothane, enflurane, and isoflurane all enhance, while sevoflurane attenuates, the Ca2+- induced Ca2+-release mechanism. However, only sevoflurane stimulates the inositol 1,4,5-triphosphate-induced Ca2+ release mechanism. Isoflurane and sevoflurane do not stimulate Ca2+ release or influence Ca2+ uptake.