Mannelli M, Pupilli C, Lanzillotti R, Ianni L, Bellini F, Sergio M
Department of Clinical Physiopathology, University of Florence, Italy.
Hypertens Res. 1995 Jun;18 Suppl 1:S79-86. doi: 10.1291/hypres.18.supplementi_s79.
Dopamine (DA) is synthesized and secreted in central as well as peripheral nervous system and in the adrenal medulla. Neuronal DA receptors, which have been characterized as D2 receptors, mediate an inhibition of adenylate cyclase and are located prejunctionally on sympathetic nerve endings and on chromaffin cells. Their pharmacological activation causes an inhibition of in vitro and in vivo norepinephrine (NE) release from sympathetic nerve terminals and an inhibition of in vitro epinephrine (E) release from the adrenal medulla. Endogenous DA, co-secreted with the other catecholamines (CA), modulates sympathetic-adrenal discharge only during high sympathetic stimulation through an autocrine mechanism, limiting excessive sympathetic adrenal discharge. Also pheochromocytoma cells synthesize and express D2 receptors. In patients with pheochromocytoma D2 antagonists cause hypertensive crises but the mechanism mediating this effect is still unknown as well as whether endogenous DA might modulate tumoral secretion.
多巴胺（DA）在中枢神经系统、外周神经系统以及肾上腺髓质中合成并分泌。已被鉴定为D2受体的神经元DA受体介导腺苷酸环化酶的抑制作用，位于交感神经末梢和嗜铬细胞的突触前部位。其药理学激活导致体外和体内交感神经末梢去甲肾上腺素（NE）释放的抑制以及体外肾上腺髓质肾上腺素（E）释放的抑制。内源性DA与其他儿茶酚胺（CA）共同分泌，仅在高交感神经刺激期间通过自分泌机制调节交感-肾上腺放电，限制过度的交感-肾上腺放电。嗜铬细胞瘤细胞也合成并表达D2受体。在嗜铬细胞瘤患者中，D2拮抗剂会引发高血压危象，但介导这种效应的机制以及内源性DA是否可能调节肿瘤分泌仍不清楚。
