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Ceramide-induced vasorelaxation: An inhibitory action on protein kinase C.

机译:神经酰胺诱导的血管舒张:对蛋白激酶C的抑制作用。

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摘要

Experiments were designed to examine the role of sphingosine, PP2A phosphatases, and protein kinase C (PKC) inhibition in mediating the vasodilatory effects of ceramide in rat thoracic aorta. Sphingosine did not cause vasorelaxation, and oleoylethanol-amine, a ceramidase inhibitor, did not affect sphingomyelinase-induced relaxation. Okadaic acid potentiated the relaxation response to ceramide. These observations rule out involvement of sphingosine and PP2A phosphatases in mediating ceramide-induced relaxation. Sphingomyelinase attenuated contractile and single-cell intracellular calcium responses to phorbol ester. Chelerythrine incubation potentiated the relaxation response to ceramide. These observations support a role for PKC inhibition in mediating the vasodilatory effects of ceramide.
机译:设计实验以检查鞘氨醇,PP2A磷酸酶和蛋白激酶C(PKC)抑制在介导神经酰胺在大鼠胸主动脉中的血管舒张作用中的作用。鞘氨醇不引起血管舒张,并且神经酰胺酶抑制剂油酰乙醇胺不影响鞘磷脂酶诱导的松弛。冈田酸增强了对神经酰胺的松弛反应。这些观察结果排除了鞘氨醇和PP2A磷酸酶在介导神经酰胺诱导的舒张中的作用。鞘磷脂酶减弱了对佛波酯的收缩和单细胞内钙反应。白屈菜红碱的孵育增强了对神经酰胺的松弛反应。这些观察结果支持PKC抑制在介导神经酰胺的血管舒张作用中的作用。

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