Honig A
Institute of Physiology, Ernst-Moritz-Arndt-University of Greifswald, German Democratic Republic.
Am J Physiol. 1989 Dec;257(6 Pt 2):R1282-302. doi: 10.1152/ajpregu.1989.257.6.R1282.
In response to acute exposure to moderate high-altitude hypoxia, mammals increase their blood hemoglobin concentration very rapidly by reducing their plasma volume. This phenomenon is caused not only by a redistribution of the body fluid volumes but also by a suppression of voluntary sodium and water intake as well as an inhibition of renal tubular sodium reabsorption with natriuresis and diuresis. This article reviews the role of the peripheral arterial chemoreceptors within the framework of the reflex mechanisms that might cause the changes in sodium and water metabolism in acute arterial hypoxia. The evidence that the peripheral arterial chemoreceptors do also influence sodium and water homeostasis in normoxia is presented. The interrelations between carotid body structure and arterial chemoreceptor reflex effects on the one hand and primary systemic hypertension on the other are discussed.
作为对急性中度高原缺氧的反应，哺乳动物通过减少血浆量非常迅速地增加其血液血红蛋白浓度。这种现象不仅是由体液量的重新分布引起的，还由自愿性钠和水摄入量的抑制以及肾小管钠重吸收的抑制伴钠尿和利尿引起。本文回顾了外周动脉化学感受器在可能导致急性动脉缺氧时钠和水代谢变化的反射机制框架内的作用。文中还给出了外周动脉化学感受器在常氧状态下也会影响钠和水平衡的证据。讨论了一方面颈动脉体结构与动脉化学感受器反射效应之间的相互关系，另一方面与原发性系统性高血压之间的相互关系。
