The effects of long-term administration of benzothiadiazine diuretics on electrolyte metabolism of hypertensive patients are ill defined. Applying results of acute changes in sodium and potassium balance to conditions of prolonged therapy has led to doubtful assumptions. Sodium loss has been believed responsible for the long-term reduction in blood pressure, whereas potassium wastage presumably represents a major untoward side-effect.
This study was designed to delineate the magnitude, frequency, and significance of biochemical alterations during long-term administration of bendroflumethiazide to nonedematous hypertensive patients.
It appears reasonable to postulate a compensatory increase in aldosterone secretion in response to sodium loss from diuretic therapy. We studied this by observing the modifying influence of an added aldosterone blocking agent, spironolactone, and of sodium and potassium chloride loading experiments.
The effects of these drugs on the blood pressure of these same patients were recorded in a collateral communication.1
Material and Methods
I. Electrolyte Balance
GRIEBLE HG, JOHNSTON LC, FULLER JB. Treatment of Arterial Hypertensive Disease with Diuretics: II. Effects on Electrolytes and Uric Acid of Bendroflumethiazide, Potassium Chloride, and Spironolactone. Arch Intern Med. 1962;110(1):34–44. doi:10.1001/archinte.1962.03620190036005
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