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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，而与平滑肌细胞的亚细胞结构无关
Rollin (30μmol·L-1), a phosphodiesterase isoenzyme Ⅳ (PDEⅣ) inhibitor, inhibited the accumulation of cyclic adenosine monophosphate (cAMP) in 30 μmol·L-1 isoproterenol The enhancement was stronger than that of PDEⅢ inhibitor (SKF94836, 30μmol·L-1), but was weaker than the isoproterenol-induced enhancement of relaxation of tracheal smooth muscle in SKF94836. 30μmol·L-1Rol or SKF94836 on 30μmol·L-1 forskolin induced tracheal smooth muscle relaxation and cAMP accumulation of almost equal degree of enhancement. Isoproterenol and forskolin, alone or in combination with SKF94836 and Rol, caused only cAMP accumulation in soluble portion of canine smooth muscle, which had no significant effect on cAMP content in granulosa. These results suggest that the regional distribution of cAMP in canine smooth muscle cells is regulated by PDEⅢ and PDEⅣ, but not with the subcellular structure of smooth muscle cells