Sodium excretion during elevation of renal venous pressure: modulation by dDAVP

J. D. Firth, A. E. Raine and J. G. Ledingham Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom. Studies were performed to determine the effects of elevation of renal venous pressure on sodium excretion by the isolated perfused rat kidney in the presence and absence of a specific V2-receptor agonist, 1-des-amino-8-D-arginine vasopressin (dDAVP), at a concentration (1 ng/ml) expected to have maximal antidiuretic activity but minor vasopressor action. In either the presence or absence of dDAVP, increments in venous pressure led to falls in perfusate flow rate and glomerular filtration rate, which became significant at an imposed pressure greater than or equal to 18.75 mmHg. In the absence of dDAVP, absolute sodium excretion fell as venous pressure increased, and there was a negative correlation between fractional sodium excretion (FENa) and renal venous pressure (RVP) within each experiment and when all data points were combined: FENa = 3.46-0.072RVP (r = -0.608, P less than 0.01). In contrast, in the presence of dDAVP, absolute sodium excretion was unchanged, and in four of five experiments FENa rose as venous pressure increased (in one it remained unchanged). Linear regression analysis of all data points showed a positive correlation between FENa and RVP: FENa = 1.27 + 0.127RVP (r = 0.392, P less than 0.05). The slopes of the two regression lines were significantly different (P less than 0.001). It is postulated that this effect of dDAVP may be mediated via changes in the distal tubular pressure response to elevation of RVP. Such an effect of vasopressin could explain the observation that the response to renal vein constriction in vivo is dependent on volume status.