The resistance to hypothiazid (hydrochlorothiazide) during the development of acute renal insufficiency (ARI) induced by glycerin injection was studied in rat experiments. Natriuretic, kaliuretic, and hydrouretic activity of the diuretic decreased two days after injection of a glycerin solution. In this period hypothiazid excretion with the urine was least. Ten days later, despite the restoration of the water- and electrolyte-excretion function of the kidneys and normalization of hypothiazid excretion with the urine, the natriuretic effect of the drug was still very poor. This is indirect evidence of the long-term affection of the receptors for the thiazid diuretics during the development of ARI. The affection remains even after the excretory function of the kidneys is restored. The high correlation between the cumulative excretion of hypothiazid with the urine and natriuresis encountered in intact animals was weaker in rats with acute renal insufficiency.
Acute Kidney Injury/drug therapy , Hydrochlorothiazide/antagonists & inhibitors , Sodium Chloride Symporter Inhibitors/antagonists & inhibitors , Acute Kidney Injury/chemically induced , Acute Kidney Injury/physiopathology , Acute Kidney Injury/urine , Animals , Diuresis/drug effects , Diuretics , Drug Evaluation, Preclinical , Drug Resistance , Electrolytes/urine , Glycerol , Hydrochlorothiazide/urine , Rats , Sodium Chloride Symporter Inhibitors/urine , Time Factors
