The natriuretic response to hydromineral imbalance.

Abstract

SUMMARY Many recent investigations of the mechanism of volume-expansion natriuresis fail to appreciate that the observed renal sodium excretion may not be dependent on an increase in intravascular volume, but rather on the infused sodium load or extracellular fluid volume expansion. With this in mind, the natriuresis of isotonic volume expansion, hypertonic saline infusion, and dehydration have a common basis: they present a relative or absolute sodium load. Lesions of forebrain periventricular tissue prevent the natriuretic response to these three states of body fluid imbalance. In this review we discuss the evidence for a common central nervous system-mediated natriuretic mechanism in response to disturbances of fluid and electrolyte balance. We also propose a role for pars intermedia-derived, proopiomelanocortin-derived peptides as humoral mediators of renal sodium excretion. Evidence from our laboratory, as well as others, provides data for a testable hypothesis to explain central nervous system-mediated natriuresis, as well as an explanation of how central nervous system lesions or neurochemical perturbations affect the renal response to body fluid imbalance. ume-expansion natriuresis agree that the natriuretic response is not correlated to an increase in intravascular volume, but rather to the infused sodium load or extracellular expansion. Intravascular volume-expansion with sodium-free solutions of hyperoncotic dextran, hyperosmotic glucose, hyperoncotic albumin, or hypotonic sodium chloride produces little increase in sodium excretion. '• 2 Expansion with saline or blood, however, challenges that produce an expansion of the extracellular fluid volume and present a sodium load, results in a significant increase in urinary sodium excretion.1 -2 The hemodynamic response to "pure" intravascular expansion, isotonic saline expansion, or volume expansion with blood is quite similar. These data suggest that an increase in

Concentrations of electrolytes, hormones, and other constituents in fresh postmortem blood and urine of fin whales (<i>Balaenoptera physalus</i>)

“…In the North Atlantic Ocean fin whales feed voraciously and accumulate fat reserves (Víkingsson 1990). When feeding, the whales take in a hefty salt load, which expands their extracellular fluid (ECF) space and intravascular volume, lowering protein and phosphorus levels; this is followed by slow shrinkage of the space during the protracted postprandial diuresis, possibly caused partly by natriuretic peptides (Gruber 1987). Postprandial diuresis, with its high initial osmolality and urinary electrolyte levels, has been described in pinnipeds and odontocetes (Malvin and Rayner 1968;Ridgway 1972), but postprandial ECF expansion has not been confirmed.…”

Regulation of salt and water balance

“…At least one ASTI may have structural similarity with some pituitary hormones (MSH, ACTH). The possibility of species differences is important because in dogs, unlike primates, cardiac denervation reduces the renal response to ECF volume expansion (Gruber 1987).…”