We have previously reported that the administration of intravenous furosemide to patients with chronic congestive heart failure (CHF) caused an increase in mean arterial pressure, an increase in systemic vascular resistance and a decrease in cardiac output before the onset of diuresis.1 These hemodynamic events were accompanied by large increases in plasma renin activity, a moderate increase in plasma norepinephrine (NE), and a small increase in plasma arginine vasopressin (AVP). We postulated on the basis of these observations that the vasoconstrictor response induced by intravenous furosemide was due to acute neurohumoral activation. It was not possible to tell from the previous investigation which of the vasoconstrictor systems might have been responsible for the increase in vascular tone, because all 3 systems were concomitantly activated. In this study, we investigated the hypothesis that the renin-angiotensin system may mediate the acute presser response to furosemide.
Bibliographical noteFunding Information:
From the Hennepin County Medical Center, Cardiology Division, 701 Park Avenue, Minneapolis, Minnesota 55415, and the University of Minnesota, Minneapolis. This study was supported by a grant-in-aid from the American Heart Association, Dallas, Texas, and by research funds from the Veterans Administration, Washington, DC. Dr. Goldsmith is an Established Investigator of the American Heart Association and CIBA-Geigy Corp., Summit, New Jersey. Manuscript received June 5, 1989; revised manuscript received and accepted August 14, 1989.