Urinary excretion of urodilatin is increased during pressure natriuresis in the isolated perfused rat kidney

Background

Treatment with urodilatin (URO; ANP-95-126), a kidney derived natriuretic peptide, may be beneficial in patients with incipient acute renal failure after cardiac surgery [1]. The findings about mechanisms regulating endogenous production and renal excretion of URO are controversial. Recent evidence suggests that urinary excretion of urodilatin (V_UROU) is increased in patients after uncomplicated cardiac surgery and positively correlated with blood pressure [2].

Objective

To determine the effects of different perfusion pressures on urine flow (VU), urinary excretion of sodium (V_NaU), potassium (V_kU) and urodilatin (V_UROU) and the concentration of urodilatin in the perfusate (P_URO) in isolated perfused rat kidneys.

Materials and methods

Kidneys from Sprague-Dawley rats were perfused for 180 min with constant perfusion pressures (80 mmHg (n = 4); 120 mmHg (n = 4)) in a closed circuit system. Samples were taken every 30 min. The concentration of urodilatin in urine and perfusate were determined by a radioimmuno-assay for raturodilatin (rURO: Immundiagnostik, Bensheim, Germany) not cross-reacting with rBNP, rCNP, rCDD/ANP-99-126 or hURO.

Results

Mean VU, V_NaU, V_kU and V_UROU were significantly higher with a perfusion pressure of 120 mmHg than with 80 mmHg (all: P < 0.05); P _URO did not change significantly.

Conclusion

Our data suggest that renal perfusion pressure and consequently mean arterial blood pressure are determinants of V_UROU. Additionally, our data underline the importance of perfusion pressure for adequate renal function; this may be especially relevant for patients at risk to develop acute renal failure after cardiac surgery.