The dopaminergic system influences the heart rhythm by inhibiting the rat cardiac sympathetic and parasympathetic neurotransmissions through activation of D₂-like receptors (encompassing the D₂, D₃, and D₄ subtypes). Whereas D₂ receptor subtype activation results in cardiac sympatho-inhibition, the dopamine receptor subtypes involved in rat cardiac vago-inhibition remain unknown. Hence, this study investigated the specific functional role of the D₂-like receptor subtypes (D₂, D₃, and/or D₄) inhibiting the rat heart cholinergic drive. For this purpose, male Wistar rats were pithed and prepared for cardiac vagal stimulation. Bradycardic responses were obtained by electrical stimulation of vagal fibres (3, 6, 9 Hz; n = 100) or i.v. acetylcholine (ACh; 1, 5, 10 μg/kg; n = 15). Expression of D₂, D₃, and D₄ receptors was studied in left and right atrium samples by PCR (n = 4). Intravenous injections of quinpirole (D₂-like agonist; 1–30 μg/kg), but not of SFK-38393 (D₁-like agonist; 1–30 μg/kg), dose-dependently inhibited the vagally induced bradycardia. The vago-inhibition induced by quinpirole (which failed to affect the bradycardia to i.v. ACh) was unchanged after i.v. injections of the antagonists L-741,626 (D₂; 100 μg/kg) or SB-277011-A (D₃; 100 μg/kg), but it was abolished by L-745,870 (D₄; 100 μg/kg). mRNA levels of D₂, D₃, and D₄ receptor subtype were detected in the left and right rat atria. Our results suggest that the quinpirole-induced vagolytic effect involves prejunctional D₄ receptor subtypes, located in the left and right atria. This provides new evidence on the relevance of D₄ receptor modulating the heart parasympathetic control.

多巴胺能系统通过激活 D ₂样受体（包括 D ₂、D ₃和 D ₄亚型）抑制大鼠心脏交感神经和副交感神经传递来影响心律。尽管 D ₂受体亚型激活导致心脏交感神经抑制，但参与大鼠心脏迷走神经抑制的多巴胺受体亚型仍然未知。因此，本研究调查了 D ₂样受体亚型（D ₂、D ₃和/或 D ₄) 抑制大鼠心脏胆碱能驱动。为此，对雄性 Wistar 大鼠进行了髓核并准备进行心脏迷走神经刺激。通过迷走神经纤维（3、6、9 Hz；n = 100）或静脉注射乙酰胆碱（ACh；1、5、10 μg/kg；n = 15）的电刺激获得心动过缓反应。D ₂、D ₃和D ₄受体的表达通过PCR在左心房和右心房样本中进行研究（n = 4）。静脉注射喹吡罗（D ₂样激动剂；1–30 μg/kg），但不是 SFK-38393（D ₁- 类似激动剂；1–30 μg/kg)，剂量依赖性地抑制迷走神经诱发的心动过缓。静脉注射拮抗剂 L-741,626 (D ₂ ; 100 μg/kg) 或 SB-277011-A (D ₃ ; 100 μg ) 后，喹吡罗诱导的迷走神经抑制（未能影响静脉注射 ACh 的心动过缓）没有改变/kg)，但它被 L-745,870 (D ₄ ; 100 μg/kg)废除。在左右大鼠心房中检测到D ₂、D ₃和 D ₄受体亚型的mRNA 水平。我们的结果表明，喹吡罗诱导的迷走神经溶解作用涉及位于左右心房的结前 D ₄受体亚型。这为 D ₄的相关性提供了新的证据 受体调节心脏副交感神经控制。