Disturbance of kidney aldosterone sensitivity and the mechanism of its development during neurodystrophy.
It has been established that neurodystrophy resulting from the sectioning of an animal's left sciatic nerve and treatment of its central stump with formalin leads to a prolonged disturbance of the water- and salt-excreting function of the kidneys. As a rule, this is expressed as oligouria and decreased excretion of sodium in the urine. The indicated changes are due to disturbance of both intra- and extrarenal mechanisms. Intrarenal mechanisms of oligouria basically involve an acute depression in filtration of primary urine, and the hyponatriuresis is due to a decrease in the sodium load of the nephron and to an increase in the tubular reabsorption of sodium. Extrarenal mechanisms implicated in the indicated changes in sodium reabsorption involve an increased concentration of mineralocorticoid hormones of the body. Further studies have shown that the hyponatriuresis which arises during neurodystrophy is related not only to the increased concentration of the above-mentioned hormones in the fluid media of the body, but also is related to a change in the kidneys' sensitivity to them.
D000450:Aldosterone; D000818:Animals; D004231:Diuresis; D007668:Kidney / Q000294:innervation* / Q000378:metabolism; D007674:Kidney Diseases / Q000378:metabolism / Q000503:physiopathology*; D009318:Natriuresis; D010523:Peripheral Nervous System Diseases / Q000503:physiopathology*; D011817:Rabbits; D012964:Sodium / Q000378:metabolism; D014882:Water-Electrolyte Balance
D000450:Aldosterone; D012964:Sodium