Changes in β-adrenergic receptor-mediated vascular response in the septic rat thoracic aorta

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The mechanism (s) underlying the inhibitory effect of anesthetics or sepsis on endothelium-dependent vasorelaxation is still controversial. This study intended to clarify how anesthetics or sepsis interfered with endothelium-mediated vasorelaxation.The volatile anesthetic halothane inhibited carbachol-induced increase in cytosolic Ca^<2+> concentration and resultant decrease in muscle tension in aconcentration-dependent manner. In addition,halothane concentration dependently inhibited nitroglycerin-induced vasorelaxation partly in a Ca^<2+>-dependent fashion. These findings strongly indicated that halothane interfered with endothelium-mediated vasorelaxation both at the NO synthetic process and at the NO-mediated vasorelaxing process. Dobutamine, a β1 adrenergic agonist, and salbutamol, a β2 adrenergic agonist, induced vasorelaxation in endothelium-intact vascular strip. In contrast, dobutamine's effect was almost abolished in endothelium-denuded strip, suggesting that dobutamine's effect was mediated by endothelium. Not only α-adrenergic receptor-mediated vasoconstriction, but β-adrenergic receptor-mediated vasorelaxation was inhibited in the septic rat aorta. Therefore, sepsis induces multifactorial inhibition on vascular relaxation.