Endocrine control of electrolyte balance during development.
The endocrine control of electrolyte balance during development is reviewed. It is suggested that the high urinary sodium excretion observed in premature infants may be secondary to the immaturity of the adrenal gland to adequately increase the secretion of aldosterone (Sulyok et al, 1979b), and to the inability of the distal tubule to respond appropriately to a rise in circulating aldosterone levels (Sulyok et al, 1979a). On the other hand, the elevated plasma aldosterone levels observed in term newborn infants may play an important role in the blunted response of the newborn kidney to saline loading (Sulyok et al, 1979a; Spitzer, 1982). The ability of ANP to induce a natriuresis and to contribute to fluid and electrolyte homeostasis during development has been investigated. It has been found that the immature kidney is less responsive to ANP than later in life (Chevalier et al, 1988; Robillard et al, 1988). On the other hand, it has been suggested that a rise in plasma ANP during the first five days of life may contribute to the physiological weight loss associated with the extracellular volume contraction occurring shortly after birth (Tulassay et al, 1987). The role of glucocorticoids, prostaglandins and the kallikrein-kinin system in regulating electrolyte balance during development is also reviewed.
Robillard
J E
JE
Smith
F G
FG
D004702:Endocrine Glands / Q000502:physiology*; D005260:Female; D006128:Growth; D006801:Humans; D011247:Pregnancy; D014882:Water-Electrolyte Balance