Taniguchi T, Fujiwara M, Lee J J, Hidaka H
J Pharmacol Exp Ther. 1979 Sep;210(3):349-53.
The positive chronotropic effect of cholera enterotoxin on isolated rabbit sinoatrial (S-A) node was investigated. This toxin produced a time and dose-related increase in pacemaker rate and cyclic adenosine 3':5'-monophosphate (cyclic AMP) levels and shifted to the left the dose-response curves of norepinephrine on the pacemaker rate and cyclic AMP content in the S-A node. Thus, the sensitivity of the S-A node to norepinephrine was increased by the toxin. These effects of the toxin were not blocked by propranolol. There was a linear relation between the increases in pacemaker rate and cyclic AMP content after application of both the toxin and norepinephrine. However, the slope of the regression line relating pacemaker rate to cyclic AMP level differed with these two agents. These results suggest that cholera enterotoxin increases pacemaker rate with activation of the adenylate cyclase system in the S-A node, but the mechanism differs from that of norepinephrine.
研究了霍乱肠毒素对离体兔窦房（S-A）结的正性变时作用。该毒素使起搏频率和环磷酸腺苷（cAMP）水平出现与时间和剂量相关的增加，并使去甲肾上腺素对S-A结起搏频率和cAMP含量的剂量-反应曲线左移。因此，该毒素增加了S-A结对去甲肾上腺素的敏感性。普萘洛尔不能阻断该毒素的这些作用。应用毒素和去甲肾上腺素后，起搏频率的增加与cAMP含量之间存在线性关系。然而，将起搏频率与cAMP水平相关联的回归线斜率在这两种药物作用下有所不同。这些结果表明，霍乱肠毒素通过激活S-A结中的腺苷酸环化酶系统来增加起搏频率，但其机制与去甲肾上腺素不同。
