Mukai T, Takagi K, Takayanagi I, Iwayama Y, Yamaguchi E
J Pharmacobiodyn. 1982 May;5(5):308-13. doi: 10.1248/bpb1978.5.308.
Relationship between contraction and cyclic AMP levels induced by BaCl2 was examined in the longitudinal smooth muscle isolated from guinea pig ileum. BaCl2 3 X 10(-3)M caused a fast initial contraction, often followed by a gradual decrease of the contractile state. There was an increase in the tissue cyclic AMP 7 min or 14 min after the application of Ba. A phosphodiesterase activator imidazole reinforced the later phase of contraction by Ba and inhibited the increase in cyclic AMP. These results indicate that there is still a positive correlation between relaxation and increase in cyclic AMP and that an inhibitory action mediated by cyclic AMP is veiled behind the Ba contraction. Furthermore, these results may be interpreted by assuming that strong Ba contraction operates a feedback mechanism and that the feedback mechanism is associated with cyclic AMP increase. Indomethacin, an inhibitor of prostaglandins synthesis, little influenced the Ba-induced increase in cyclic AMP and rather inhibited the Ba contraction. Propranolol, a beta-adrenergic blocking agent, failed to exert influence on the Ba contraction. Based on these facts, it is suggested that the increase in cyclic AMP is not mediated by prostaglandins or catecholamines.
在从豚鼠回肠分离出的纵行平滑肌中,研究了氯化钡诱导的收缩与环磷酸腺苷(cAMP)水平之间的关系。3×10⁻³M的氯化钡引起快速的初始收缩,随后收缩状态常逐渐下降。施加氯化钡后7分钟或14分钟,组织中的环磷酸腺苷增加。磷酸二酯酶激活剂咪唑增强了氯化钡引起的后期收缩,并抑制了环磷酸腺苷的增加。这些结果表明,松弛与环磷酸腺苷增加之间仍存在正相关,并且环磷酸腺苷介导的抑制作用在氯化钡收缩背后被掩盖。此外,这些结果可以通过假设强烈的氯化钡收缩启动了一种反馈机制,且该反馈机制与环磷酸腺苷增加相关来解释。前列腺素合成抑制剂吲哚美辛对氯化钡诱导的环磷酸腺苷增加影响很小,反而抑制了氯化钡收缩。β-肾上腺素能阻滞剂普萘洛尔对氯化钡收缩没有影响。基于这些事实,表明环磷酸腺苷的增加不是由前列腺素或儿茶酚胺介导的。