Ferré F
Life Sci. 1986 Nov 17;39(20):1893-900. doi: 10.1016/0024-3205(86)90300-0.
The effect of dopamine on adenylate cyclase activity was investigated in slices of human term placentas. Dopamine elicited a dose-dependent stimulation of cAMP formation with a ED50 value of about 1 X 10(-6)M dopamine and an increase of 110% over the control with 1 X 10(-4)M dopamine. (-)-Epinephrine and (-)-norepinephrine also increased placental cAMP formation. Apomorphine displayed a slight but non-significant stimulatory effect while bromocriptine was not effective. SCH 23390, a selective antagonist of dopamine D1 receptors caused a dose-dependent decrease of the dopamine activation. In contrast, the dopamine increase of cAMP was unaffected by beta- and alpha-adrenergic blocking drugs and by the D2 selective antagonist, (-)-sulpiride. These data indicate that dopamine stimulates cAMP formation in human term placenta through a specific mechanism via D1 dopaminergic receptors positively coupled to adenylate cyclase.
研究了多巴胺对足月人胎盘切片中腺苷酸环化酶活性的影响。多巴胺对环磷酸腺苷（cAMP）的生成有剂量依赖性刺激作用，其半数有效剂量（ED50）值约为1×10⁻⁶M多巴胺，使用1×10⁻⁴M多巴胺时，cAMP生成量比对照组增加110%。（-）-肾上腺素和（-）-去甲肾上腺素也能增加胎盘cAMP的生成。阿扑吗啡显示出轻微但无统计学意义的刺激作用，而溴隐亭则无效。多巴胺D1受体的选择性拮抗剂SCH 23390可导致多巴胺激活作用呈剂量依赖性降低。相反，cAMP的多巴胺增加不受β-和α-肾上腺素能阻断药物以及D2选择性拮抗剂（-）-舒必利的影响。这些数据表明，多巴胺通过与腺苷酸环化酶正偶联的D1多巴胺能受体，经特定机制刺激足月人胎盘cAMP的生成。
