Salt-Appetite Mechanism for Controlling Extracellular Fluid Sodium Concentration and Volume

Salt-Appetite Mechanism for Controlling Extracellular Fluid Sodium Concentration and Volume

Maintenance of normal extracellular fluid volume and sodium concentration requires a balance between sodium excretion and sodium intake. In modern civi-lizations, sodium intake is almost always greater than necessary for homeostasis. In fact, the average sodium intake for individuals in industrialized cultures eating processed foods usually ranges between 100 and 200 mEq/day, even though humans can survive and function normally on 10 to 20 mEq/day. Thus, most people eat far more sodium than is necessary for home-ostasis, and there is evidence that our usual high sodium intake may contribute to cardiovascular disorders such as hypertension.

Salt appetite is due in part to the fact that animals and humans like salt and eat it regardless of whether they are salt-deficient. There is also a regulatory component to salt appetite in which there is a behavioral drive to obtain salt when there is sodium deficiency in the body. This is particularly important in herbivores, which nat-urally eat a low-sodium diet, but salt craving may also be important in humans who have extreme deficiency of sodium, such as occurs in Addison’s disease. In this instance, there is deficiency of aldosterone secretion, which causes excessive loss of sodium in the urine and leads to decreased extracellular fluid volume and decreased sodium concentration; both of these changes elicit the desire for salt.

In general, the two primary stimuli that are believed to increase salt appetite are (1) decreased extracellular fluid sodium concentration and (2) decreased blood volume or blood pressure, associated with circulatory insuffi-ciency. These are the same major stimuli that elicit thirst.

        The neuronal mechanism for salt appetite is analo-gous to that of the thirst mechanism. Some of the same neuronal centers in the AV3V region of the brain seem to be involved, because lesions in this region frequently affect both thirst and salt appetite simultaneously in animals. Also, circulatory reflexes elicited by low blood pressure or decreased blood volume affect both thirst and salt appetite at the same time.