Effects of Low and High Sodium Chloride Diets and Furosemide Administration on Cardiac Function, Plasma Electrolyte Concentrations, and the Renin-Angiotensin-Aldosterone System

Congestive heart failure is commonly treated with a low sodium diet and diuretic. The purpose of this treatment is the reduction of preload, or blood volume presented to the diseased cardiac muscle. The purpose of this study was to assess the roles of dietary sodium and furosemide on cardiac function, plasma electrolyte concentrations, and the renin-angiotensin-aldosterone system, in healthy canines. Twenty mixed-breed canines were allotted to one of four groups, Group I - Dogs fed low sodium diet (0.08% sodium), Group II - Dogs fed high sodium diet (1.0% sodium), Group III - Dogs fed low sodium (0.08%) and treated with furosemide (2 mg/kg orally (PO) every twelve hours (BID)), and Group IV - Dogs fed high sodium (1.0%) and furosemide ( 2 mg/kg PO BID). Cardiac function was assessed via echocardiography on days 0, 21,and 53. Plasma electrolyte concentrations were measured on days 0, 21, and 35. Activation of the renin-angiotensin-aldosterone system was evaluated on days 0, 21, 35, and 53. Low and high sodium diet with and without furosemide treatment did not alter cardiac function, plasma sodium, or plasma potassium concentrations. However, furosemide treatment combined with a low sodium diet resulted in the lowest plasma chloride concentrations, on days 21 and 35 (p<0.05). Furthermore, furosemide treatment resulted in significant alterations in the renin-angiotensin-aldosterone system, on days 21, 35, and 53, (p < 0.0001). Furosemide treatment significantly increased renin activity and aldosterone concentration. The interaction between furosemide and the low sodium diet yielded a greater increase in plasma renin activity and plasma aldosterone concentrations than furosemide administration with the high sodium diet. These results suggest direct activation of the renin-angiotensin-aldosterone system by furosemide. Future research is warranted in congestive heart failure subjects, due to the adverse affects of decreased plasma chloride concentrations and activation of the renin-angiotensin-aldosterone system.