Endogenous digoxin-like factor raises blood pressure and protects against digitalis toxicity

Digoxin-like immunoreactive factor (DLIF) is an endogenous natriuretic material which causes diuresis and natriuresis after salt or fluid loading and which may play a pathogenetic role in various hypertensive states. In order to study the cardiovascular effects of DLIF, we administered partially purified material (500 ng/kg) iv to normal rats. DLIF administration caused a significant rise in blood pressure, induced a brisk diuresis, and slowed the heart rate. In addition, DLIF protected against digitalis toxicity. While iv digoxin, 1 mg/kg, uniformly produced lethal arrhythmias, administration of DLIF 15 min prior to digoxin infusion consistently protected against arrhythmias. These findings support the theory that DLIF may play a role in hypertension. In addition, DLIF may compete with digoxin for cardiac receptors.