Abstract

We have previously found in urine from salt-loaded rats and in patients with heart failure, a new natriuretic factor which has, in part, the biological profile of loop diuretic drugs. In patients with congestive heart failure, it is not known whether the activation of this factor is related to the impairment in systolic contractility. The aim of this study was to determine the differences in Cotransport Inhibitory Factor (C.I.F.) response between patients with or without left ventricular dysfunction. Twenty one patients were included in this study (16 men and 5 women, mean age 53, range 38 to 72). All treatments were maintained except loop diuretics. Left ventricular ejection fraction (LVEF) was measured by contrast or isotopic angiography (range 14–74%). Plasma and urine C.I.F. levels were measured by potency of the samples to inhibit cotransport fluxes in Madin and Darby canine kidney (MDCK) cells, and in human erythrocytes. Cotransport inhibition in urine and plasma was correlated with LVEF as shown in figure ( * and ** = p < 0.0002). This study shows that the degree of C.I.F activation is related to the level of LV dysfunction and that besides ANF, C.I.F. could playa key role in diuresis and natriuresis control in congestive heart failure.

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