Belmaker R H, Ebstein R P, Schoenfeld H, Rimon R
Psychopharmacology (Berl). 1976 Sep 17;49(2):215-7. doi: 10.1007/BF00427293.
Administration of epinephrine in man has been shown previously to lead to a rise in plasma cyclic AMP levels by activation of the beta-adrenergic-stimulated adenylate cyclase. Therapeutic doses of lithium in humans block the epinephrine-induced rise in plasma cyclic AMP levels, suggesting that lithium inhibits beta-adrenergic adenylate cyclase. In contrast, ten subjects receiving haloperidol, a druh also effective in the treatment of mania, show a mean rise in plasma cyclic AMP levels after epinephrine administration and the magnitude of the response is the same as for non-drug treated individuals. These findings are discussed in relation to the possible pharmacological mechanisms of action of lithium and haloperidol in the control of mania.
先前已表明,在人体中注射肾上腺素会通过激活β-肾上腺素能刺激的腺苷酸环化酶导致血浆环磷酸腺苷(cAMP)水平升高。治疗剂量的锂在人体中会阻断肾上腺素诱导的血浆cAMP水平升高,这表明锂会抑制β-肾上腺素能腺苷酸环化酶。相比之下,十名接受氟哌啶醇(一种对治疗躁狂症也有效的药物)治疗的受试者在注射肾上腺素后,血浆cAMP水平平均升高,且反应程度与未接受药物治疗的个体相同。结合锂和氟哌啶醇在控制躁狂症方面可能的药理作用机制对这些发现进行了讨论。