磷酸二酯酶同工酶Ⅲ和Ⅳ调节气管平滑肌环腺苷酸的区域化分布

Compartments of cyclic adenosine monophosphate are regulated differentially by phosphodiesterase Ⅲ and Ⅳ in canine trachealis 1

磷酸二酯酶同工酶Ⅳ（ＰＤＥⅣ）抑制剂咯利普兰（Ｒｏｌ，３０μｍｏｌ·Ｌ－１）对３０μｍｏｌ·Ｌ－１异丙肾上腺素所致的犬气管平滑肌环腺苷酸（ｃＡＭＰ）积聚的增强作用比ＰＤＥⅢ抑制剂氰胍哒嗪（ＳＫＦ９４８３６，３０μｍｏｌ·Ｌ－１）要强，但对异丙肾上腺素所致的犬气管平滑肌松弛的增强作用比ＳＫＦ９４８３６要弱．３０μｍｏｌ·Ｌ－１Ｒｏｌ或ＳＫＦ９４８３６对３０μｍｏｌ·Ｌ－１福斯科林所致的犬气管平滑肌松弛与ｃＡＭＰ积聚的增强作用程度几乎相等．异丙肾上腺素，福斯科林单独或与ＳＫＦ９４８３６，Ｒｏｌ合用都仅引起犬气管平滑肌的可溶部ｃＡＭＰ积聚，对颗粒部ｃＡＭＰ含量无明显影响．上述结果提示犬气管平滑肌存在着ｃＡＭＰ的区域化分布，它受ＰＤＥⅢ，ＰＤＥⅣ的调节。

Rolipram (Rol, 30 μmol·L -1 ), an inhibitor of phosphodiesterase Ⅳ (PDEⅣ), produced a greater potentiation of isoprenaline (Iso, 30 μmol·L -1 ) induced cAMP accumulation in canine trachealis than that of siguazodan (SKF94836, 30 μmol·L -1 ), an inhibitor of PDEⅢ, while a reverse was observed for relaxation of trachealis strips induced by Iso. SKF94836 and Rol produced an almost identical potentiation of forskolin (For, 30 μmol·L -1 ) induced trachealis relaxation and cAMP accumulation. Iso and For alone or the combination with SKF94836 and Rol respectively increased the contents of soluble, but not particulate cAMP. These results suggest that the compartmentation of cAMP in canine trachealis may be regulated differentially by PDEⅢ and PDEⅣ, but be not due to the differences in particulate or soluble subcellular compartments.