INHIBITION OF NA-K-CL COTRANSPORT FLUXES AND SALIDIURETIC ACTION BY AN URINARY EXTRACT OF SALT-LOADED RATS

We previously found a potent inhibitor of the Na-K-Cl cotransport syst em in urines from salt-loaded rats (C.I.F. = cotransport inhibitory fa ctor, ref. 1). Here we extracted an urinary fraction (approximate to 1 parts per thousand urine dry weight), free from immunoreactive A.N.P. and digoxine activity, which : (i) potently inhibited cotransport flu xes in MDCK (Madin and Darby canine kidney] cells and in human erythro cytes, (ii) inhibited Na+-dependent chloride/bicarbonate exchange with 2-3 times less potency than cotransport and (iii) strongly increased natriuresis and diuresis after i.v. infusion in rats with no significa nt change in kaliuresis (salidiuretic action reduced by probenecid). T herefore, C.I.F. seems to be a new natriuretic factor with part, but n ot all the biological profile of loop diuretic drugs.