[Response and endocrine mechanisms in the kidney effected by sodium chloride].

Abstract

The results of experiments on white rats, consuming different quantities of NaCl, show that excessive sodium chloride load increases osmolarity of blood plasma mainly due to excessive accumulation of Cl- in the blood. At the same time urine osmolarity increases by a factor of 10 due to the rise of water reabsorption and a fall in reabsorption of osmotical active substances such as sodium, potassium, chlorides, phosphates and other ions showing tendency to the glomerulus filtration rate rise. This testifies to the priority of osmoregulation over ionoregulation. NaCl injection causes a fall in difference of Na+ and Cl- concentrations in the blood plasma due to Na+ deposition by tissues, which leads to extracellular metabolic acidosis. Kidneys respond to it by a decrease of the urine pH and increase of excretion of hydrogen ions in the form of titrated acids and ammonium, as well as by removal of chloride ions which are not connected with sodium. The conclusion is made that kidneys' function of acid-excretion depends first of all on the acid-base status of extracellular fluids and not on intracellular pH. Concentration of corticotropin in the blood increases in the case of sodium deficiency as well as in the excess of sodium. Deficiency of Na+ intensifies activity of the renin-angiotensin-aldosterone system and decreases ADH secretion, while salt load produces just the opposite effect. The role of the hormones in kidneys' compensatory reaction to excessive NaCl load is discussed.