Water Balance

Osmoreceptors (Figure 4-10A) located in the hypothalamus (and also in the carotid artery) are capable of sensing increased concentrations of solutes, particularly Na+. This leads to a secretion of vasopressin, which stimulates renal tubular water reabsorption. At the same time, the thirst center in the hypothalamus, which is linked to the osmoreceptor, is stimulated with a concomitant increase in water consumption.

1. Renal Relationships of K+ and Na+

Although Na+ is the principal extracellular cation and K+ is the principal intracellular cation, the metabolism and homeostasis of these monovalent cations are closely interrelated. It is essential to life that serum K+ levels be maintained within normal limits (3.8-5.4 meq/ liter), so that the normal K+ concentration of 150-160 meq/liter of intracellular water can be supported.

The homeostatic control of K+ is not regulated as stringently as that of Na+. An important endocrine contribution to K+ homeostasis is the major stimulatory effects of K+ on aldosterone secretion. Aldosterone in turn acts on the renal tubules to restore plasma K+ to normal by enhancing the renal tubular excretion of K+. Also, the falling levels of plasma K+ are known to stimulate renin secretion, which in turn will ultimately lead to the normal action of aldosterone upon increasing Na+ reabsorption. It is to be emphasized that there is no stoichiometric relationship between Na+ reabsorption and K+ excretion; thus, K+ excretion may increase prior to an effect on Na+, and normally the aldosterone effect on K+ diminishes before its action on Na+ terminates. Finally, K+ can stimulate the secretion of insulin. This in turn leads to the promotion by insulin of glucose and K+ entry into cells, which also has the consequence of lowering blood K+.

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