Abstract
Na deficiency was induced in calves by unilateral exteriorization of the parotid duct, the continual loss of alkaline saliva from the body to the environment causing negative Na balance. The metabolic effect of negative Na balance was seen in statistically significant reduction in plasma Na and blood bicarbonate, together with marked acidosis and reduced plasma osmolality. The homoeostatic response to Na depletion was associated with a reversal of Na/K ratio in parotid saliva and a reduction of the rate of secretion. Appetite diminished. The extracellular fluid was halved as marked diuresis developed with considerable weight loss. Urinary and fecal Na was reduced to 0. On restoration of Na balance by allowing the calves to drink sodium bicarbonate solutions the metabolic deviations were eliminated. During Na depletion the parotid gland was able to respond to transient reflex stimulation by increasing flow rate and the Na concentration of the saliva. When Na depleted, the calves became restless and agitated and would run from the home pen to the operant procedure stand. The Na depleted animals readily pressed a panel for sodium bicarbonate rewards in direct proportion to the degree of Na imbalance. When the balance was restored the motivation to work for sodium bicarbonate disappeared. The motivation which developed during Na depletion was directed specifically towards the Na ion. In Na depletion the glottal Na taste receptors might develop an enhanced threshold for Na ions because of the reduced Na content of the saliva. This effect would be abolished when the content of Na was restored in saliva. The correlation of operant reactions and Na depletion suggests that the consequential metabolic effects activate changes in the CNS. The metabolic changes which develop in parallel with the severity of the Na deficit appear to be able to evoke behavioral changes with increase in salt appetite directed towards restoration of Na balance.