Acute and chronic effects of benzthiazide in dogs

Abstract

Benzthiazide has a rapid onset of action characterized by a significant increase in urinary excretion of sodium and chloride and a smaller increase in potassium in acute experiments. Benzthiazide causes a hyponatremia in 2–4 days in dogs at dosage levels of 0.2 mg/kg to 4.0 mg/kg. This response corrected itself with continued administration if the dog was on a regular diet. Benzthiazide caused a similar decrease in plasma sodium with a much slower return to normal in dogs on a low-sodium diet. In dogs on a regular diet benzthiazide did not cause a hypopotassemia or an alkalosis with continued administration for periods as long as 4 weeks. All dogs showed a constant weight or gain in weight. A hypopotassemia of sudden onset developed in dogs on a low-sodium low-potassium diet and benzthiazide which continued without an associated alkalosis. Dogs on the low-sodium low-potassium diet developed a similar hypopotassemia without mecation. Anorexia was observed in dogs receiving medication on a low-sodium low-potassium diet. This was related to the diet since it also appeared in control dogs. Benzthiazide produced increased sodium and chloride excretion in the presence of either metabolic acidosis of metabolic alkalosis. Benzthiazide was effective in reversing the sodium-retaining effect of 9α-fluoro-hydrocortisone. Benzthiazide did not produce a change in the responsiveness of the arterioles to norepinephrine in either normal or nephrectomized dogs. Benzthiazide did not produce a change in plasma potassium concentration in bilaterally nephrectomized dogs.