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The mechanism of vasodilation induced by propofol was investigated using isolated rat thoracic aortic rings. Aortic rings were precontracted with potassium chloride (KCl) (40 mM) or phenylephrine (PE) (3 × 10−8to 3 × 10−7M) in the presence and absence of intact endothelium. Propofol produced similar concentration-dependent relaxation in aortic rings with and without endothelium regardless of whether they were precontracted with KCl or PE. The relaxation response to propofol was significantly greater in KCl-contracted aortic rings than in PE-contracted aortic rings. The propofol concentration producing 50% relaxation from the contracted state (RC50) was lower in aortic rings contracted with KCl than with PE, both with (5 × 0.6 × 10−5M vs 8.3 × 5.7 × 10−4M, P < 0.001) and without intact endothelium (3.9 × 0.5 × 10−5M vs 7.2 × 3.8 × 10−4M, P < 0.001). Propofol inhibited the Ca2+-induced contractions of aortic rings exposed to Ca2+-free media and depolarized with KC1 (40 mM, 100 mM) in a dose-dependent manner. These effects are similar to those produced by verapamil. Propofol (5 × 10−5M) had minimal effect on the intracellular Ca2+release elicited by PE (10−5M). We conclude that vasodilation produced by propofol is not endothelium-dependent but is likely due to blockade of voltage-gated influx of extracellular Ca2+.