Huang M H, Sylvén C, Horackova M, Armour J A
Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
Am J Physiol. 1995 Aug;269(2 Pt 2):R318-24. doi: 10.1152/ajpregu.1995.269.2.R318.
Effects elicited by adenosine and substance P on ventricular sensory endings of 14 dorsal root ganglion afferent neurons were studied in situ in anesthetized dogs. Sensory-field application of adenosine (1 microM) increased the activity of these neurons by 179%. Application of a nonspecific adenosine antagonist to epicardial sensory fields suppressed ongoing activity in all 14 neurons by 39%. Application of an A1- or A2-adenosine-receptor antagonist suppressed activity generated by 10 of these neurons by 44 and 59%, respectively. Adenosine applied after A1- or A2-receptor blockade increased activity in 10 neurons by 131 and 145%, respectively, indicating that A1- and A2-receptor effects were not additive. Application of substance P (1 microM) to identified sensory fields increased activity in 12 of these neurons by 169%, whereas application of a substance P-receptor antagonist reduced activity generated by these neurons by 75%. Myocardial ischemia increased activity of nine neurons associated with left ventricular sensory fields by 320%, an effect that was counteracted by the nonspecific adenosine-receptor antagonist. It is concluded that A1- and A2-adenosine receptors, as well as substance P receptors, are present on ventricular epicardial sensory nerve endings of dorsal root ganglion neurons that are tonically active during normal states, becoming further activated during ischemia.
在麻醉犬身上，对14个背根神经节传入神经元的心室内感觉末梢进行了原位研究，观察腺苷和P物质对其产生的效应。在感觉野施加腺苷（1微摩尔）可使这些神经元的活动增加179%。在心外膜感觉野施加非特异性腺苷拮抗剂可使所有14个神经元的持续活动抑制39%。施加A1或A2腺苷受体拮抗剂可分别使其中10个神经元产生的活动抑制44%和59%。在A1或A2受体阻断后施加腺苷可使10个神经元的活动分别增加131%和145%，表明A1和A2受体的效应并非相加。对已确定的感觉野施加P物质（1微摩尔）可使其中12个神经元的活动增加169%，而施加P物质受体拮抗剂可使这些神经元产生的活动减少75%。心肌缺血可使与左心室感觉野相关的9个神经元的活动增加320%，这种效应可被非特异性腺苷受体拮抗剂抵消。结论是，A1和A2腺苷受体以及P物质受体存在于背根神经节神经元的心外膜感觉神经末梢上，这些神经元在正常状态下呈紧张性活动，在缺血时会进一步激活。
