Clinical disorders of water metabolism

Abstract

The osmotic concentration of body fluids in man is maintained remarkably constant between 286 and 294 mOsm/kg H 2 O despite large variations in water intake. This flexibility is made possible by the operation of a thirst-neurohypophyseal-renal feedback system. This system is characterized by a very sensitive osmotic control of thirst and vasopressin 1 secretion (1 to 2% threshold) and by the action of this hormone on its target organ, the kidney. In the kidney vasopressin alters the water permeability of the collecting duct epithelium thereby modulating the rate of renal excretion of water. Thus, in the face of increased water intake, the small reduction in the tonicity of body fluids suppresses vasopressin release and leads to maximal urinary dilution. The excretion of the excess water thus occurs with restoration of plasma osmolality to normal. Conversely, if water intake is limited, a small increase in plasma osmolality activates the organism's water conserving mechanism by stimulating thirst and increasing the secretion of vasopressin. Vasopressin then increases collecting duct water permeability and thereby facilitates the reabsorption of water and the concentration of urine. It follows, therefore, that impairments in either maximal diluting or concentrating abilities will markedly decrease the range of water intake that the patient can tolerate. The disturbances in renal water excretion and the resultant alterations in body tonicity are the subjects of this paper.