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

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.