Roll of cellular Signalling systems on intraocular pressure regulation mechanisms.

为了阐明环磷酸腺苷（cAMP）系统与肌醇磷脂转换系统之间的相互作用，我们研究了改变肌醇磷脂转换系统的药物如何影响睫状体上皮细胞中cAMP系统，在培养的鸡胚睫状体上皮细胞中观察到cAMP在异丙肾上腺素、毛喉素和氟化钠刺激下的增加。用200 nM佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）预处理培养的细胞，对异丙肾上腺素诱导的cAMP增加有42%的抑制作用。用PKC抑制剂H-7（50 μ M）孵育细胞，用200 μ M PMA预处理，再用异丙肾上腺素刺激，可减弱对cAMP升高的抑制作用，用200 μ M PMA预处理的细胞对forskolin诱导的cAMP升高抑制12%。200 nM PMA预处理对NaF刺激的培养细胞内cAMP的增加无抑制作用，提示cAMP系统的抑制是由PKC的激活引起的。β-肾上腺素能受体是PKC的作用点。

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.