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From the present investigation it appears that quinethazone produces diuresis by blocking tubular reabsorption of sodium, chloride and water. It induces a greater loss of chloride than of sodium and therefore a prolonged administration of the diuretic agent may lead to a metabolic hypochloremic alkalosis. It produces in healthy individuals an increased renal excretion of the nitrogenous substances (urea and creatinine). It is a diuretic characterized by a fast onset of action which, however, is of a longer duration than that of chlorothiazide. Quinethazone causes, in comparison to chlorothiazide, a greater loss of water, sodium and chloride and a smaller of potassium. The diuretic action of quinethazone is not potentiated, except a little, by simultaneous inhibition of carbonic anhydrase activity. Therefore, the simultaneous administration of quinethazone and acetazolamide does not produce a notable increase of the diuretic action of the former. The prolonged administration of quinethazone does not cause any remarkable changes in scrum electrolytes. Nevertheless, it increases the serum uric acid level without any clinical symptoms of gout. Quinethazone possesses no notable diuretic action when given to patients suffering from chronic renal failure; on the contrary, it causes an increased retention of urea and so leads to azotliemia or aggravates such an existing condition. Quinethazone administered at a dose of 50 mg per day causes no remarkable side effects. © 1966 S. Karger AG, Basel. |
