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Correction of Dilutional Hyponatremia in Severe Chronic Heart Failure by Converting-Enzyme Inhibition

[+] Article, Author, and Disclosure Information

Grant support: Dr. Packer is the recipient of a Young Investigator's Research Award (R23-HL-25055) from the National Heart, Lung, and Blood Institute.

▸Requests for reprints should be addressed to Milton Packer, M.D.; Division of Cardiology, Mount Sinai Medical Center, 1 Gustave Levy Place; New York, NY 10029.

New York, New York

© 1984 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1984;100(6):782-789. doi:10.7326/0003-4819-100-6-782
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To determine the effects of vasodilator and inotropic therapy on hyponatremia in patients with severe heart failure, we measured serum sodium concentration before and after treatment with captopril (70 patients), hydralazine (42 patients), prazosin (22 patients), and amrinone (19 patients), while diuretic dosages were kept constant. Serum sodium concentration increased only in hyponatremic patients treated with captopril (131.2±0.5 to 135.9±0.5 SE; p < 0.001), but not during therapy with the other agents and not in patients with normal serum sodium concentration before treatment. Serum sodium began to rise 48 hours after the initiation of captopril therapy and reached its peak after 14 to 16 days. Correction of hyponatremia was related to functional interference with the renin-angiotensin system, but not to changes in renal function, serum potassium concentration, body weight, or the magnitude of hemodynamic or clinical improvement. These findings support experimental evidence that the renin-angiotensin system is important in the pathogenesis of hyponatremia in patients with severe heart failure treated with diuretics.





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