LOW-DOSE ATRIAL-NATRIURETIC-FACTOR AND FUROSEMIDE IN EXPERIMENTAL ACUTE CONGESTIVE-HEART-FAILURE

This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize card iorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemi de upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the cont rol group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Gr oup 1; N = 6), plasma ANF increased after the onset of CHF; GFR and so dium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2 (N = 6), furosemide in acute CHF inc reased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3 ; N = 6) in acute CHF were associated with a maintenance of GFR, no ac tivation of the RAAS, and potentiation of furosemide-induced natriures is. In summary, these studies demonstrate that furosemide potently inc reases sodium excretion in acute CHF, but with a decrease in GFR and a ctivation of the RAAS. Low-dose ANF in acute CHF with furosemide maint ains GFR, attenuates activation of the RAAS, and potentiates natriures is.