Chitravanshi V C, Calaresu F R
Department of Physiology, University of Western Ontario, London, Canada.
Brain Res. 1992 Jun 26;583(1-2):308-11. doi: 10.1016/s0006-8993(10)80040-x.
To investigate the effects of dopamine (DA) on vagal efferent activity, DA was microinjected into the right nucleus ambiguus (NA) in rats. Experiments were done in 19 urethane anaesthetized, artificially ventilated spinal (C1) rats. Sites in the right NA containing cardioinhibitory neurons were identified by observing a marked and reproducible decrease in heart rate (HR; 64.9 + 2.8 bpm; n = 36) elicited by microinjecting L-glutamate (GLU; 1.5. nmol in 10 nl). No decreases in arterial pressure (AP) were obtained at these sites. Microinjection of DA (1-15 nmol in 10 nl) into 24 of these 36 sites caused a dose-dependent decrease in HR. The responses to 1 nmol and 3 nmol DA were blocked by (+/-)-sulpiride, a specific D2 receptor antagonist (0.1 nmol in 10 nl). A higher dose of (+/-)-sulpiride (1 nmol in 10 nl) was required to block the responses to 15 nmol of DA. Bradycardia elicited by even the lowest amount of DA (1 nmol) was not blocked by SCH-23390, a specific D1 receptor antagonist. These experiments demonstrate that the bradycardia caused by microinjection of DA into the NA is due to the excitation of dopamine D2 receptors present on vagal preganglionic cardioinhibitory neurons controlling HR.
为研究多巴胺（DA）对迷走神经传出活动的影响，将DA微量注射到大鼠右侧疑核（NA）中。实验在19只经乌拉坦麻醉、人工通气的脊髓（C1）大鼠上进行。通过观察微量注射L-谷氨酸（GLU；10 nl中含1.5 nmol）引起的心率（HR；64.9±2.8次/分钟；n = 36）显著且可重复的下降，来确定右侧NA中含有心抑制神经元的部位。在这些部位未观察到动脉压（AP）下降。在这36个部位中的24个部位微量注射DA（10 nl中含1 - 15 nmol）导致心率呈剂量依赖性下降。对1 nmol和3 nmol DA的反应可被特异性D2受体拮抗剂（±）-舒必利（10 nl中含0.1 nmol）阻断。阻断对15 nmol DA的反应需要更高剂量的（±）-舒必利（10 nl中含1 nmol）。即使是最低剂量（1 nmol）的DA引起的心动过缓也不能被特异性D1受体拮抗剂SCH-23390阻断。这些实验表明，将DA微量注射到NA中引起的心动过缓是由于控制心率的迷走神经节前心抑制神经元上存在的多巴胺D2受体被激活所致。
