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CARDIOVASCULAR ANESTHESIA

Thiopental Induces Contraction of Rat Aortic Smooth Muscle Through Ca²⁺ Release from the Sarcoplasmic Reticulum

Department of Anesthesia, Kyoto University Hospital, Kyoto, Japan

Address correspondence and reprint requests to Taijiro Enoki, MD, Department of Anesthesia, Kyoto University Hospital, Kyoto 606-8507, Japan.

Little is known about the mechanism of thiopental-induced contraction in vascular smooth muscle. This study aimed to clarify this question by conducting isometric tension experiments and ⁴⁵Ca²⁺ flux measurements in endothelium-denuded rat aortic rings. Thiopental induced a concentration-dependent contraction under basal tension. This contraction was enhanced when rings were precontracted with phenylephrine in the presence of verapamil. In Ca²⁺-free solution, thiopental-induced contraction was reduced but not abolished with high concentrations. Ca²⁺ store depletion with a maximum dose of caffeine in Ca²⁺-free solution further reduced the contraction by subsequent thiopental. Ca²⁺ store depletion with thapsigargin completely abolished contraction by thiopental. ⁴⁵Ca²⁺ influx experiment in the presence of verapamil showed that thiopental could not induce any Ca²⁺ influx with or without phenylephrine prestimulation. The ⁴⁵Ca²⁺ efflux experiment showed more evidence of thiopental-induced Ca²⁺ release, which was abolished by thapsigargin. In conclusion, thiopental induces contraction in rat aortic smooth muscle by releasing Ca²⁺ from the sarcoplasmic reticulum without Ca²⁺ influx.

Implications: This is the first study providing evidence that thiopental-induced vascular contraction is caused by Ca²⁺ release from the sarcoplasmic reticulum of the smooth muscle.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999