Altered regulation of atrial natriuretic peptide in essential hypernatremia

Hypothalamic osmoreceptor dysfunction resulting in hypodipsia and altered regulation of vasopressin secretion is well established as the pathogenetic mechanism in the syndrome of 'essential hypernatremia'. However, little is known about the secretory pattern of atrial natriuretic peptide (ANP) in this syndrome. Therefore, we assessed ANP regulation by determining ANP concentrations in a patient manifesting this syndrome of essential hypernatremia during several well-established experimental protocols. The serum ANP level was within normal limits despite severe euvolemic hypernatremia (serum Na+ 163 mEq/l) during one of the many admissions and remained unchanged following normalization of serum Na+. Furthermore, a decline in serum ANP instead of an appropriate rise was noted when hypernatremia (serum Na+ 152 mEq/l) was induced by either hypertonic (3%) saline infusion or following a high-Na+ (300 mEq/day) diet for several days (serum Na+ 161 mEq/l). Similarly, exogenous pitressin administration failed to cause a rise in ANP, although an appropriate fall in ANP concentration occurred following fluid deprivation. Therefore, it is apparent that ANP regulation may be significantly altered in essential hypernatremia. However, further studies are required to define whether it plays a role in the pathogenesis of hypernatremia in this syndrome.