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 system in urines from salt-loaded rats (C.I.F. = cotransport inhibitory factor, ref. 1). Here we extracted an urinary fraction (approximately 1% urine dry weight), free from immunoreactive A.N.P. and digoxin activity, which: (i) potently inhibited cotransport fluxes in MDCK (Madin and Darby canine kidney] cells and in human erythrocytes, (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 significant change in kaliuresis (salidiuretic action reduced by probenecid). Therefore, C.I.F. seems to be a new natriuretic factor with part, but not all the biological profile of loop diuretic drugs.