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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.
A. Hönig (Fri,) studied this question.