Diuretic and antihypertensive actions of furosemide.

Abstract

Furosemide (4 - chloro - N - (2 - furyl - methyl) - 5 - sulfamoylanthranilic acid) caused a prompt increase in sodium, potassium, and chloride excretions in patients with chronic congestive heart failure. Doses of 50, 100, and 200 mg orally produced progressively increasing diuretic responses. When given over a period of one week to patients with essential hypertension, furosemide in doses of 100 to 200 mg orally per day caused a significant decrease in systolic and diastolic pressure. A significant lowering of blood pressure was also demonstrated in hypertensive patients treated with furosemide over a period of one year. Biochemical alterations during furosemide administration included elevation of fasting blood sugar levels in patients with diabetes mellitus, increased uric acid concentrations, and lowering of plasma potassium levels. All biochemical changes were reversible when the drug was discontinued. No evidence of hematologic or hepatic dysfunction was observed in 16 patients who received furosemide in a daily dose of 40 to 160 mg over a 52-week period. Although furosemide has been recommended primarily for the treatment of edema refractory to other forms of therapy, long-term studies indicate that the drug is also capable of maintaining patients with chronic congestive heart failure without producing serious systemic toxicity.