Abstract
The effects of aclarubicin on phosphatidylinositol hydrolysis and contractile responses were investigated in isolated rat aorta. In the aclarubicin-pretreated aorta, the basal level of [ 3H]inositol monophosphate accumulation was significantly lower whereas [ 3H]phosphoinositide formation was significantly higher than in the saline-pretreated control aorta. Phenylephrine-, 5-hydroxytryptamine- and sodium fluoride-stimulated increases in [ 3H]inositol monophosphate accumulation were also significantly reduced in the aclarubicin-treated aorta compared to the control. Contractile forces induced by 5-hydroxytryptamine and sodium flouride were merkedly diminished in the aclarubicin-treated aorta. These results suggest that aclarubicin inhibits phosphatidylinositol hydrolysis at a level of phospholipase C activation, which is involved in the reduction of agonist-induced contraction of rat aorta.
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