AJP - Renal Physiology, Vol 256, Issue 5 776-F779, Copyright © 1989 by American Physiological Society
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.
