Dutta-Roy A K, Kahn N N, Sinha A K
Receptor Research Lab, Rowett Research Institute, Bucksburn, Aberdeen, Scotland, U.K.
Life Sci. 1991;49(16):1129-39. doi: 10.1016/0024-3205(91)90560-x.
Prostaglandin E1/I2 and insulin receptors of human erythrocyte and platelet are capable of modulating each other's activity. This modulation of the receptor activity and number in one system by a second receptor system in human platelet and erythrocyte seems to be beneficial. Insulin increases the PGE1 binding to platelets and thereby enhances the platelet antiaggregatory action of prostaglandin by increasing cyclic AMP levels. Similarly, PGE1 increases insulin binding to human erythrocyte, and thereby reduces the optimum concentration of insulin for a maximal reduction in membrane microviscosity. During ischemia the reduced response of platelets to the inhibitory effect of PGE1 or PGI2 relates to the impaired PGE1/I2 receptor activity. Treatment of these platelets with insulin at physiological concentrations can normalise the PGE1/I2 receptor activity. This review focuses on the relationship between the two receptor systems in human blood cells.
前列腺素E1/I2与人类红细胞和血小板的胰岛素受体能够相互调节对方的活性。在人类血小板和红细胞中,一个受体系统对另一个受体系统的活性和数量的这种调节似乎是有益的。胰岛素增加血小板对PGE1的结合,从而通过提高环磷酸腺苷水平增强前列腺素的血小板抗聚集作用。同样,PGE1增加胰岛素与人类红细胞的结合,从而降低使膜微粘度最大程度降低所需的胰岛素最佳浓度。在缺血期间,血小板对PGE1或PGI2抑制作用的反应降低与PGE1/I2受体活性受损有关。用生理浓度的胰岛素处理这些血小板可使PGE1/I2受体活性恢复正常。本文综述聚焦于人类血细胞中这两种受体系统之间的关系。