Consolim-Colombo F M, Hay M, Smith T C, Elizondo-Fournier M, Bishop V S
Department of Physiology, University of Texas Health Science Center at San Antonio 78284-7756, USA.
Am J Physiol. 1996 Jul;271(1 Pt 2):R34-41. doi: 10.1152/ajpregu.1996.271.1.R34.
Angiotensin II (ANG II) and arginine vasopressin (AVP) act on area postrema (AP) neurons to modulate the baroreflex. Because activation of AP neurons by either ANG II or AVP increases intracellular free Ca2+ concentrations ([Ca2+]i), the goal of this study was to analyze the factors affecting the [Ca2+]i responses to ANG II and AVP. Neurons were recovered from 14- to 16-day old rats and studied after 8-14 days in culture by use of the microscopic digital image analysis for fura 2-loaded cells. The effects of ANG II (100 nM) and AVP (100 nM) on [Ca2+]i were determined in normal (2 mM) and low (< 10 nM) extracellular Ca2+ concentrations. In 143 of 240 neurons, ANG II increased [Ca2+]i 4.65-fold after 20 s, and a similar response was observed in the absence of extracellular Ca2+ (3.65-fold after 20 s). After 60 s of observation, steady-state levels of increased [Ca2+]i were still present under both conditions. Pretreatment with AT1 antagonist or pertussis toxin abolished the response to ANG II. AVP also increased [Ca2+]i (3.6-fold at peak, 20 s) in normal and low extracellular Ca2+. Pretreatment with AVP V1 antagonist or pertussis toxin abolished the response to AVP. This study indicates that ANG II-induced increases in [Ca2+]i are independent of extracellular Ca2+ concentrations and involve the activation of AT1 receptors and a pertussis toxin-sensitive G protein. Although AVP affects a fewer number of AP neurons, the mechanisms of activation are also independent of extracellular Ca2+ concentration and are mediated by a pertussis toxin-sensitive G protein.
血管紧张素II（ANG II）和精氨酸加压素（AVP）作用于最后区（AP）神经元以调节压力反射。由于ANG II或AVP激活AP神经元会增加细胞内游离钙离子浓度（[Ca2+]i），本研究的目的是分析影响[Ca2+]i对ANG II和AVP反应的因素。从14至16日龄大鼠中分离神经元，在培养8至14天后，通过对加载fura 2的细胞进行显微数字图像分析来进行研究。在正常（2 mM）和低（<10 nM）细胞外钙离子浓度下，测定ANG II（100 nM）和AVP（100 nM）对[Ca2+]i的影响。在240个神经元中的143个中，ANG II在20秒后使[Ca2+]i增加4.65倍，在无细胞外钙离子的情况下也观察到类似反应（20秒后增加3.65倍）。观察60秒后，两种条件下[Ca2+]i增加的稳态水平仍然存在。用AT1拮抗剂或百日咳毒素预处理可消除对ANG II的反应。AVP在正常和低细胞外钙离子条件下也增加[Ca2+]i（峰值时为3.6倍，20秒）。用AVP V1拮抗剂或百日咳毒素预处理可消除对AVP的反应。本研究表明，ANG II诱导的[Ca2+]i增加与细胞外钙离子浓度无关，涉及AT1受体的激活和一种百日咳毒素敏感的G蛋白。虽然AVP影响的AP神经元数量较少，但其激活机制也与细胞外钙离子浓度无关，并由一种百日咳毒素敏感的G蛋白介导。
