Regulation of Renal Aquaporins and Sodium Transporters During Vasopressin-Escape in the Rat

Abstract

Several clinical conditions, e.g., congestive heart failure and cirrhosis are associated with inappropriately elevated vasopressin levels relative to serum osmolality (Bichet et al., 1992). In addition, ectopic production of vasopressin-like substances (usually by tumors) can produce inappropriate antidiuresis. This disorder is known as the Syndrome of Inappropriate Antidiuretic Hormone (vasopressin) secretion (SIADH). As expected, inappropriately elevated plasma vasopressin levels will often result in water retention and hyponatremia. Eventually patients go through a physiological process known as “vasopressin-escape” in which they begin to excrete a higher volume of more dilute urine, despite continually high levels of circulating vasopressin. This escape process helps to reduce water retention and more symptomatic hyponatremia. Until recently little was known about the molecular mechanisms underlying escape.