Aclarubicin inhibits phosphatidylinositol hydrolysis and contraction of rat aorta.
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 fluoride were markedly 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.
Wakabayashi
I
I
Department of Hygiene, Hyogo College of Medicine, Japan.
Sakamoto
K
K
Hatake
K
K
Tanaka
H
H
D015250:Aclarubicin / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects; D006868:Hydrolysis; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D010716:Phosphatidylinositols / Q000037:antagonists & inhibitors* / Q000378:metabolism / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012701:Serotonin / Q000494:pharmacology; D012969:Sodium Fluoride / Q000494:pharmacology
D010716:Phosphatidylinositols; D012701:Serotonin; D015250:Aclarubicin; D012969:Sodium Fluoride