AJP - Regulatory, Integrative and Comparative Physiology, Vol 250, Issue 6 973-R979, Copyright © 1986 by American Physiological Society
Renal opiate receptor mediation of renin secretion to renal nerve stimulation in the dog
S. Koyama and H. Hosomi
The present study was designed to evaluate renal opiate receptor mediation
of the renin secretion response to electrical stimulation of the renal
nerves in the pentobarbital sodium-anesthetized dog by use of the opiate
agonist leucine-enkephalin (Leu-enk) and the opiate antagonist naloxone. In
all animals studied, left kidneys were pump perfused at a constant renal
blood flow. Renal perfusion pressure (RPP) and glomerular filtration rate
(GFR) were unaltered at a stimulation frequency of 1.0 Hz; however, renin
secretion rate (RSR) increased significantly in the nontreated group.
High-frequency renal nerve stimulation (10 Hz) increased RPP and decreased
GFR. RSR at the high-frequency stimulation was significantly augmented in
the nontreated group. Renal arterial infusion of either Leu-enk (25
micrograms X kg-1 X min-1) or naloxone (7 micrograms X kg-1 X min-1) did
not alter base-line levels of renal hemodynamics and RSR and did not
produce significant changes in these variables even when renal nerves were
stimulated at the low frequency; however, Leu-enk inhibited RPP and RSR
responses to the high-frequency stimulation, and naloxone augmented these
responses. Phentolamine (13 micrograms X kg-1 X min-1) prevented renal
hemodynamic responses to the renal nerve stimulation, whereas RSR responses
to the stimulation were unaffected. Propranolol (8 micrograms X kg-1 X
min-1) resulted in decreases in RSR at the renal nerve stimulation despite
the presence of changes in renal hemodynamics similar to the other groups.
The results indicate that intrarenal opiate receptors may participate in
inhibiting renal secretion of renin mediated by the renal nerves when renal
vasoconstriction and reduction of GFR occurred at the high-frequency
stimulation.
