Meisheri K D, Diamond J, McNeill J H
Eur J Pharmacol. 1981 Jul 17;73(1):81-3. doi: 10.1016/0014-2999(81)90148-5.
This study examines a possibility that high-K+ depolarization induced inhibition of cAMP accumulation by beta-adrenoceptor stimulation (observed in our previous studies) is mediated by depolarization induced release of acetylcholine. Rat uterine strips were depolarized by high-K+ solution with or without atropine. Isoproterenol produced similar degrees of relaxation and increases in cAMP levels in depolarized smooth muscle with or without atropine. It is suggested that the release, if any, of acetylcholine from smooth muscle depolarization is not the primary cause of the observed inhibition of cAMP accumulation.
本研究探讨了一种可能性，即高钾去极化诱导的β-肾上腺素能受体刺激所致环磷酸腺苷（cAMP）积累的抑制作用（在我们之前的研究中观察到）是由去极化诱导的乙酰胆碱释放所介导的。在有或没有阿托品的情况下，用高钾溶液使大鼠子宫肌条去极化。无论有无阿托品，异丙肾上腺素在去极化的平滑肌中产生相似程度的舒张以及cAMP水平升高。这表明，平滑肌去极化所释放的乙酰胆碱（如果有释放的话）并非所观察到的cAMP积累抑制的主要原因。
