Meisheri K D, Ruegg J C
Pflugers Arch. 1983 Dec;399(4):315-20. doi: 10.1007/BF00652759.
cAMP (10(-6) - 10(-4) M) produced a dose-dependent relaxation of Ca2+-induced contraction in the guinea-pig taenia coli skinned with 1% Triton X-100. At 0.53 microM Ca2+ and 0.05 microM calmodulin (CaM), cAMP (10(-4) M) produced a maximal relaxation of 75% (pH 6.7; 25 degrees C). Increasing Ca2+ (0.8 microM) or CaM (0.37 microM) reduced cAMP-induced relaxation to 25 and 5% respectively. At high CaM (5 microM), cAMP-induced relaxation could be completely inhibited by as low as 0.25 microM Ca2+. Furthermore, small increases in Ca2+ or CaM could effectively reverse the cAMP-induced relaxation in the continuous presence of cAMP. These results demonstrate that small modulations in the Ca2+-calmodulin activity have a strong effect on the ability of cAMP to produce a direct relaxing effect on the contractile proteins in skinned fiber. It is suggested that the effects of cAMP on the cellular mechanisms that lower cytoplasmic free Ca2+ concentration may act as the important determinants of the extent of the direct inhibitory effect of cAMP on the contractile elements. These two mechanisms may act in concert in this fashion to effect cAMP-induced relaxation in smooth muscle during beta-adrenergic stimulation.
环磷酸腺苷（cAMP，10⁻⁶ - 10⁻⁴ M）对用1% Triton X - 100剥除肌膜的豚鼠结肠带的Ca²⁺诱导收缩产生剂量依赖性舒张作用。在0.53微摩尔/升Ca²⁺和0.05微摩尔/升钙调蛋白（CaM）条件下，cAMP（10⁻⁴ M）产生的最大舒张率为75%（pH 6.7；25℃）。增加Ca²⁺（0.8微摩尔/升）或CaM（0.37微摩尔/升）可分别将cAMP诱导的舒张率降低至25%和5%。在高CaM（5微摩尔/升）时，低至0.25微摩尔/升的Ca²⁺就能完全抑制cAMP诱导的舒张。此外，在持续存在cAMP的情况下，Ca²⁺或CaM的小幅增加可有效逆转cAMP诱导的舒张。这些结果表明，Ca²⁺ - 钙调蛋白活性的微小调节对cAMP对剥除肌膜纤维收缩蛋白产生直接舒张作用的能力有强烈影响。提示cAMP对降低细胞质游离Ca²⁺浓度的细胞机制的作用可能是cAMP对收缩元件直接抑制作用程度的重要决定因素。这两种机制可能以这种方式协同作用，在β - 肾上腺素能刺激期间影响平滑肌中cAMP诱导的舒张。
