Dinh Thu T, Flynn Francis W, Ritter Sue
Programs in Neuroscience, Washington State University, Pullman, WA 99164-6520, USA.
Am J Physiol Regul Integr Comp Physiol. 2006 Oct;291(4):R870-9. doi: 10.1152/ajpregu.00094.2006. Epub 2006 May 4.
To better understand the involvement of hindbrain catecholamine neurons in hypovolemia-induced secretion of AVP, we injected antidopamine beta-hydroxylase saporin (DSAP) or unconjugated saporin (SAP) control solution into the hypothalamic paraventricular nucleus (PVH) of anesthetized rats to retrogradely lesion catecholamine neurons innervating magnocellular areas of the hypothalamus. Subsequently, hypotensive hypovolemia was induced by remote blood withdrawal (4.5 ml, 1 ml/min) using an intra-atrial catheter. Blood was sampled at 2, 5, 20, and 50 min after onset of blood withdrawal. The AVP response was severely impaired by DSAP. Peak responses at 50 min were 51 pg/ml in SAP control and 17 pg/ml in DSAP-lesioned rats, indicating the importance of catecholamine neurons for this response. We also measured AVP responses to osmotic challenge induced by administration of hypertonic saline (1 M, 15 ml/kg, sc) and to insulin-induced hypoglycemia. Osmotic challenge increased AVP levels, but the response was not impaired by DSAP, indicating that AVP neurons were not damaged by the DSAP injection. Insulin-induced hypoglycemia did not increase AVP levels in either DSAP- or SAP-treated rats. However, the same dose of insulin increased food intake and corticosterone secretion in SAP controls, and these responses were profoundly impaired by DSAP. Thus catecholamine neurons are required for both the AVP response to hypotensive hypovolemia and for feeding and corticosterone responses to hypoglycemia. Lack of an AVP response to insulin-induced hypoglycemia in intact rats therefore indicates that responses to hypovolemia and hypoglycemia are mediated by different catecholamine neurons under distinct sensory controls.
为了更好地理解后脑儿茶酚胺神经元在低血容量诱导的血管加压素（AVP）分泌中的作用，我们将抗多巴胺β-羟化酶皂草素（DSAP）或未结合的皂草素（SAP）对照溶液注入麻醉大鼠的下丘脑室旁核（PVH），以逆向损伤支配下丘脑大细胞区的儿茶酚胺神经元。随后，使用心房内导管通过远程放血（4.5 ml，1 ml/min）诱导低血压性低血容量。放血开始后2、5、20和50分钟采集血液样本。DSAP严重损害了AVP反应。在50分钟时，SAP对照组的峰值反应为51 pg/ml，而DSAP损伤大鼠为17 pg/ml，表明儿茶酚胺神经元对该反应的重要性。我们还测量了AVP对高渗盐水（1 M，15 ml/kg，皮下注射）诱导的渗透刺激以及对胰岛素诱导的低血糖的反应。渗透刺激增加了AVP水平，但该反应未被DSAP损害，表明AVP神经元未因DSAP注射而受损。胰岛素诱导的低血糖在DSAP或SAP处理的大鼠中均未增加AVP水平。然而，相同剂量的胰岛素增加了SAP对照组的食物摄入量和皮质酮分泌，而这些反应被DSAP严重损害。因此，儿茶酚胺神经元对于AVP对低血压性低血容量的反应以及对低血糖的进食和皮质酮反应都是必需的。因此，完整大鼠对胰岛素诱导的低血糖缺乏AVP反应表明，对低血容量和低血糖的反应是由不同的儿茶酚胺神经元在不同的感觉控制下介导的。
