ENDOGENOUS SODIUM-POTASSIUM-CHLORIDE COTRANSPORT INHIBITOR IN CONGESTIVE-HEART-FAILURE

Objectives. This study sought to evaluate the relation, if any, betwee n fluid overload in congestive heart failure (CHF) and a newly discove red endogenous natriuretic factor acting like loop diuretic drugs: cot ransport inhibitory factor (CIF). Background. The humoral mechanisms r egulating volume overload in CHF are not fully understood, Therefore, we investigated whether there is a role for CIF in this pathologic con dition, Methods. Plasma and urinary CHF levels were investigated in 23 patients with chronic CHF and compared with changes in plasma atrial natriuretic peptide (ANP), Twelve patients without CHF served as contr ol subjects. Results. CHF was associated with a highly significant thr eefold increase in both plasma CIF levels (mean +/- ST) 7,10 +/- 3,01 vs, 2,28 +/- 0,92 U/ml, p < 0.0001) and urinary CIF excretion (7,849 /- 3,600 vs. 2,351 +/- 1,297 U/day, p < 0.0001) with respect to patien ts without CHP. CIF increased as a function of impairment in left vent ricular ejection fraction (r = -0.703, p < 0,0001) and the severity of clinical status. Plasma ANP was also increased in patients with CRF, although to a lesser extent (68%, p = 0.0501) than plasma CIF, and was also significantly correlated with left ventricular ejection fraction (r = -0.552, p = 0.0004). Conclusions. Plasma and urinary CIF activit ies were strongly acid very significantly increased in chronic CHF. Ln addition to ANP, this long-term natriuretic agent may be of potential importance in reducing fluid overload in CHF.