A number of studies have shown that rats with congestive heart failure (CHF) have increased protein levels of the vasopressin-regulated water channel AQP2 even during conditions with unchanged circulating levels of vasopressin (AVP), suggesting an increase in the sensitivity of the AVP type-2 (V₂) receptor in experimental CHF. The present study was aimed at investigating AVP signaling in rats with moderate CHF (left ventricular end diastolic pressure >10 mmHg; normal plasma AVP levels) induced by ligation of the left anterior descending coronary artery. Sham-operated rats were used as controls. Western blotting analyses revealed an increased abundance of AQP2 in renal cortex (+ 33±9 % of Sham; p<0.05) and in inner medulla (IM) (+54±15% of Sham; p<0.05) in CHF rats when compared to sham operated controls. Dose response studies on isolated collecting ducts (CD's) showed an increased accumulation of cAMP in response to AVP in CHF rats when compared to controls. V₂-receptor surface binding studies in isolated IMCD's showed a marked and comparable AVP-induced V₂-receptor internalization in response to AVP in both CHF and control rats. As expected V₂-receptor surface binding remained low after AVP challenge in control rats. In contrast to this, V₂-receptor surface binding returned to pre-AVP levels within 30 minutes in the CHF rats indicating an obtained recycling ability of the V₂-receptor in CHF. Together the results indicate the presence of an increased AVP sensitivity in the CD's from CHF rats, associated with an acquired recycling ability of the V₂-receptor.