The Carotid Bodies and Sodium Metabolism

Abstract

Mild hypoxia induces polyuria and, in those lowlanders who tolerate rapid ascent to high altitude well, there may be a diuresis that lasts for days. This brings about a contraction of extracellular and plasma volume producing the “haemoconcentration” characteristic of early exposure to high altitude (Asmussen and Nielsen 1945; Berger et al. 1949; Heath and Williams 1989, pp 182–183). Since the osmotic pressure of extracellular fluid is precisely controlled, the reduced volume is achieved by a negative sodium balance. Many subjects, on the other hand, who ascend mountains become oliguric during the first few hours of their exposure to the hypobaric hypoxia. At the same time there is a redistribution of water in the body, with a shift of water into the extracellular compartment, leading to acute mountain sickness and predisposing to high-altitude pulmonary and cerebral oedema (Heath and Williams 1989, pp 196–201). This regulation of sodium and water excretion is brought about by the interaction of several hormones listed below and particularly by aldosterone and antidiuretic hormone. Honig (1989) has suggested that the natriuretic response to the hypobaric hypoxia of high altitude may be influenced in addition by the carotid bodies. It has been appreciated for many years that the haemo-concentration of early exposure to the mountain environment may play a part in acclimatisation to high altitude, for it enables the blood to carry more oxygen per unit volume. Thus a natriuretic response to hypoxia not only reduces the risk of pulmonary or cerebral oedema, but also increases oxygenation of the tissues. The possible involvement of the carotid bodies in the regulation of sodium and water metabolism in hypoxia is discussed in this chapter. The reduction in plasma volume which accompanies acclimatisation to hypoxia can be attained by two mechanisms: a voluntary reduction in dietary intake of salt and water and their increased excretion by the kidneys (Honig 1989).