Abstract

Recent studies suggest that the endogenous digitalis-like substance (DLS) implicated in the pathogenesis of low renin hypertension in animals and humans may be a steroidal dienolide derivative. One of these derivatives, bufalin (aglycone), inhibits Na+,K+-ATPase (1) and has recently been shown in our laboratory to have some of the physiological characteristics expected of a DLS (2). For example, infusion of bufalin into the brachial artery of the anesthetized dog increases vascular resistance and blocks K+ vasodilation while it potentiates norepinephrine vasoconstriction (Fig. 1). When bufalin is administered intravenously in the dog, increases in heart rate, dP/dt, and arterial blood pressure ensue (Fig. 2). In some animals (3/7) post-infusion natriuresis and diuresis occurs. Intravenous infusion in the rat likewise produces increases in blood pressure, heart rate, and dP/dt, and marked diuresis, natriuresis and kaliuresis (3) during and post-infusion. The present study in the anesthetized dog has been designed to examine the mechanism for the post-infusion natriuresis and diuresis seen with bufalin.

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