Previous studies have demonstrated a role for atrial natriuretic peptide (A
NP) in mediating the acute increase in urinary sodium excretion by the rema
ining kidney following unilateral nephrectomy (UNX). We have now set out to
determine whether the kallikrein-kinin system is involved in mediating the
renal effects of ANP following UNX. We did this in circumstances in which
the release of endogenous ANP was suppressed by prior removal of the right
atrial appendage. In anaesthetized Sprague-Dawley sham atrial appendectomiz
ed rats, UNX resulted in a two-fold increase in urinary excretion of sodium
(from 1.14 +/- 0.27 to 2.65 +/- 0.54 mu eq/min; P < 0.05) whereas glomerul
ar filtration rate did not change significantly. Fractional excretion of li
thium, an index of proximal tubular handling of sodium, increased and fract
ional distal reabsorption of sodium declined (+17 +/- 9 and -1.6 +/- 0.4% r
espectively; both P < 0.05 vs sham UNX group). Urinary kallikrein excretion
rose by 7.2 +/- 2.8 nKat/min from a basal value of 15.2 +/- 1.7 nKat/min (
P < 0.05 vs sham UNX group). No significant change in electrolyte excretion
was detected after sham UNX. The natriuretic response to UNX was abolished
in right atrial appendectomized rats (from 1.58 +/- 0.25 to 1.45 +/- 0.24
mu eq/min; not significant; not significant vs UNX in sham atrial appendect
omized rats and vs sham UNX animals). So were the changes in both proximal
and distal tubular reabsorption of sodium. Furthermore, urinary kallikrein
excretion failed to increase significantly in this group (by 3.6 +/- 1.7 nK
at/min from a basal value of 18.3 +/- 2.6 nKat/min; not significant vs UNX
in sham atrial appendectomized rats and vs sham UNX animals). These observa
tions confirm that ANP may be an important mediator of the natriuretic resp
onse to UNX. They suggest that the kallikrein-kinin system may play a role
as a mediator of the renal action of ANP following UNX. Med Sci Res 27:583-
586 (C) 1999 Lippincott Williams & Wilkins.