大鼠胃底对血小板活化因子（PAF）收缩反应的机制。II. PAF诱导的磷脂酰肌醇代谢转换和脱敏作用。

Mechanism of the contractile response to platelet-activating factor (PAF) of the rat stomach fundus. II. PAF-induced phosphatidylinositol turnover and desensitization.

Kamata K, Arai Y, Kasuya Y

Department of Pharmacology, School of Pharmaceutical Sciences, Hoshi University, Tokyo, Japan.

Gen Pharmacol. 1993 Nov;24(6):1337-41. doi: 10.1016/0306-3623(93)90416-u.

Abstract

Accumulation of [3H]-inositol phosphates (IPs) was slightly enhanced by PAF in a concentration-dependent manner, but the accumulation was very small as compared with that induced by carbachol. 2. The levels of [32P]-phosphatidic acid which is transformed from diacylglycerol (DAG) were increased by treatment with PAF or with carbachol. 3. PAF-induced contraction was significantly reduced by treatment with phorbol 12-myristate 13-acetate (PMA). 4. These results suggest that while PAF slightly stimulates the turnover of phosphatidylinositol (PI) in the rat stomach fundus, this response may not be responsible for the PAF-induced contractile response, and that the desensitization induced by repeated application of PAF may be due to the activation of protein kinase C.

摘要

血小板活化因子（PAF）以浓度依赖的方式使[3H]-肌醇磷酸（IPs）的积累略有增强，但与卡巴胆碱诱导的积累相比非常小。2. 由二酰基甘油（DAG）转化而来的[32P]-磷脂酸水平通过PAF或卡巴胆碱处理而升高。3. 用佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）处理可显著降低PAF诱导的收缩。4. 这些结果表明，虽然PAF在大鼠胃底中轻微刺激磷脂酰肌醇（PI）的周转，但这种反应可能与PAF诱导的收缩反应无关，并且重复应用PAF诱导的脱敏可能是由于蛋白激酶C的激活。