Effects of mineralocorticoids on Na+ and K+ excretion in the adrenalectomized rat

JD Horisberger, J Diezi - American Journal of Physiology …, 1983 - journals.physiology.org
JD Horisberger, J Diezi
American Journal of Physiology-Renal Physiology, 1983journals.physiology.org
The short-term effects (within 4 h) of low doses of intravenous aldosterone or
deoxycorticosterone on potassium and sodium urinary excretion were studied by clearance
techniques in 24-h adrenalectomized, anesthetized male rats. All animals were substituted
with a glucocorticoid (dexamethasone; plasma concentration approximately 6 nM) to
maintain normal glomerular filtration rate. The mineralocorticoid effects were studied under
various conditions of sodium and potassium load. Mineralocorticoid administration uniformly …
The short-term effects (within 4 h) of low doses of intravenous aldosterone or deoxycorticosterone on potassium and sodium urinary excretion were studied by clearance techniques in 24-h adrenalectomized, anesthetized male rats. All animals were substituted with a glucocorticoid (dexamethasone; plasma concentration approximately 6 nM) to maintain normal glomerular filtration rate. The mineralocorticoid effects were studied under various conditions of sodium and potassium load. Mineralocorticoid administration uniformly resulted in antinatriuresis, starting within 30-60 min and, at the peak effect, amounting to 1-2% sodium fractional excretion. The level of antinatriuresis was directly related to the control sodium excretion before aldosterone administration. Mineralocorticoids induced a significant kaliuresis in all groups except one, the one receiving the lowest sodium load. The aldosterone-induced kaliuresis was also related to the sodium load and the control fractional sodium excretion level and was simultaneous with the beginning of the reduced sodium excretion. In control, mineralocorticoid-deprived rats, kaliuresis was not enhanced by increasing the sodium load. Control as well as mineralocorticoid-treated rats responded by an increased kaliuresis following an acute potassium load and by a decreased kaliuresis after 3 days of low potassium diet.
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