AJP - Renal Physiology, Vol 244, Issue 4 392-F398, Copyright © 1983 by American Physiological Society
Endogenous opioids and electrolyte excretion after contralateral renal exclusion
J. Ribstein and M. H. Humphreys
Acute reductions in functioning renal mass result in increases in both
sodium (U Na V) and potassium (U K V) excretion by the contralateral kidney
(CK). We studied the role of endogenous opioids in this response. In
control experiments acute unilateral nephrectomy (AUN) increased U Na V
from 1,788 +/- 1,125 (SD) to 3,939 +/- 1,819 and U K V from 1,385 +/- 561
to 2,254 +/- 832 neq/min by the CK (P less than 0.005 for both); similar
results occurred in rats undergoing acute unilateral ureteral occlusion
(UUO). These increases occurred without overall change in GFR or mean
arterial pressure. In rats receiving a continuous infusion of the
opiate-receptor antagonist naloxone (0.3 mg . kg-1 . h-1) neither AUN nor
UUO produced significant alterations in U Na V or U K V by the CK; naloxone
infusion by itself did not alter GFR or basal rates of cation excretion. A
separate group of rats was made tolerant to morphine by subcutaneous
implantation of pellets containing 75 mg morphine base. In these rats, AUN
also failed to produce any increase in U Na V or U K V by the CK. The
results suggest that acute reductions in functioning renal mass produced by
either AUN or UUO stimulate cation excretion by the remaining kidney
through reflex pathways that involve opiate receptors.
