Roll of cellular Signalling systems on intraocular pressure regulation mechanisms.

我们研究了改变肌醇磷脂转化系统的药物如何影响睫状体上皮细胞的腺苷3‘：5’-环磷酸(CAMP)系统，以阐明cAMP系统和肌醇磷脂转化系统之间的相互作用。在培养的鸡胚睫状体上皮细胞中观察到异丙肾上腺素、Forsklin或NaF刺激cAMP增加。蛋白激酶C(PKC)激动剂佛波酯(PMA)对异丙肾上腺素引起的cAMP升高有42%的抑制作用。当用5OuM H-7孵育时，PKC抑制剂用2OOnti PMA预处理，再用异丙肾上腺素刺激，对cAMP升高的抑制作用减弱，2OOnM PMA可抑制Forsklin诱导的cAMP升高12%。在NaF刺激的培养细胞中，经20OOnM PMA预处理后，cAMP的升高没有受到抑制，提示cAMP系统的抑制是由PKC的激活引起的。-肾上腺素能受体被认为是PKC的致病点。

We studied how drugs that alter the inositol phospholopid turnover system affected the adenosine 3' : 5'-cyclic monophosphate(cAMP)system in ciliary epithelial cells to clarify a cross-talk between cAMP system and inositol phospholipid turnover system.The cAMP increases were observed in cultured chick embryo ciliary epithelial cells stimulated with isoproterenol, forskolin or NaF. The cultured cells pretreated with 2OOnM phorbol 12myristate 13-acetate(PMA), a protein kinase C(PKC)activator showed 42% inhibition of the cAMP increase induced by isoproterenol. When cultured cells incubated with 5OuM H-7, a PKC inhibitor were pretreated with 2OOnti PMA and stimulated with isoproterenol, the inhibitory effect on cAMP increase was reduced.The cultured cells pretreated with 2OOnM PMA showed 12% inhibition of the cAMP increase induced by forskolin. No inhibition of the cAMP increase was noted in the cultured cells stimulated with NaF after 2OOnM PMA pretreatment.These findings suggest that inhibition of the cAMP system is caused by the activation of PKC. -adrenergic receptor was regarded as the affected point of PKC.