What Is the Importance of Salt Appetite?

WHAT IS THE IMPORTANCE OF SALT APPETITE? ALASTAIR R. MICHELE* Truth is rarely pure and never simple.—Oscar Wilde. [1] What is the importance of salt appetite? The question seems too simple to be worth raising, yet the obvious answer remains far from satisfactory . I have no problem with the idea that sodium appetite is innate and that it is intensified by severe deficits in a quantitative fashion [2—5]. My problem is with the idea that the evolutionary selection pressure which sustains sodium appetite as such a widespread phenomenon— especially among herbivores—relates to sodium status alone. Supposedly the reason is that sodium-depleted soils produce sodiumdepleted vegetation and hence sodium-depleted animals. It is not that simple [6, 7]. I am sure that it does happen, for example in the interior of large continents, far removed from oceans or from salt deposits [2], but I believe it is the exception, certainly not the rule. Low-sodium diets do not necessarily equate with sodium-depleted animals if obligatory losses and nutritional requirements are low. In the simplest terms, the question I want to raise with regard to salt appetite is "What problem does it solve; what is its place among the mechanisms which regulate body sodium?" Regulation ofBody Sodium Sodium has two main functions in the body: 1. To act as the "osmotic skeleton" of extracellular fluid (ECF), enabling it to maintain its volume despite the osmotic effect ofthe fixed solutes in intracellular fluid (ICF). This manuscript is based on a paper presented to the 11th International Conference on the Physiology of Food and Fluid Intake at Oxford, July, 1993. *Professor of applied physiology and comparative medicine, Department of Large Animal Medicine and Surgery, Royal Veterinary College, University of London, Hawkshead Lane, North Mymms, Hatfield, Herts AL9 7TA, England.© 1994 by The University of Chicago. All rights reserved. 0031-5982/94/3704-0882$01.00 Perspectives in Biology andMedicine, 37, 4 ¦ Summer 1994 | 473 2. To provide concentration gradients which underlie the co-transport of solutes such as glucose and amino acids (e.g., in the proximal nephron and the small intestine) and also facilitate the movement of water, the provision of intracellular potassium, movement of other cations and anions, and the establishment of potential differences across cell membranes. The latter are the basis of excitability and further influence the transmembrane distribution of both cations and anions. The main mechanism establishing sodium gradients across cell membranes is the "sodium pump" (Na-K ATP'ase). While the mainstream of physiological research on sodium regulation has focused on the renal-adrenal defence against depletion, the 1980s have seen a major shift in emphasis towards the mechanisms protecting the body against excess salt [8]. This followed the determination of de Wardener [9] in championing the importance of natriuretic hormones, and the work of others, notably de Bold [10], in establishing the existence of both atrial natriuretic peptide (ANP) and circulating inhibitors of active sodium transport (which probably originate in the brain and bind to the same receptors as cardiac glycosides) [8]. Meanwhile it has also emerged that, at least in some herbivores, the gut, rather than the kidney, is arguably the main regulator of sodium balance [11, 12]. Thus the colon, like the distal nephron, is able to reduce sodium losses virtually to zero under the influence of adrenal mineralocorticoids (aldosterone ). This means that provided dermal losses are minimal (as they are in most ruminants), obligatory losses of sodium, hence dietary maintenance requirements, are extremely low [7]. Aldosterone is not the main influence on renal sodium excretion since most sodium is reabsorbed in the proximal tubule, which is not aldosterone -responsive; nevertheless, proximal reabsorption is appropriately increased during ECF "volume depletion" and reduced during volume expansion. Changes in proximal reabsorption, however, affect the delivery of sodium to the remaining segments of the nephron and, for example , inadequate delivery to the distal nephron may restrict the excretion of potassium, despite the kaliuretic effect of aldosterone [8, 13]. Thus severe sodium depletion causes enhanced proximal reabsorption of sodium , reduced distal delivery, and thereby a fall in potassium excretion, whereas milder deficits, by promoting aldosterone secretion, enhance not only renal but also colonic potassium excretion...