AJP - Regulatory, Integrative and Comparative Physiology, Vol 246, Issue 2 228-R235, Copyright © 1984 by American Physiological Society
Attenuation by prostaglandins of adrenergically induced renal vasoconstriction in anesthetized rats
K. Inokuchi and K. U. Malik
We have investigated the role of prostaglandins (PG) in the modulation of
adrenergic neuroeffector events by examining the effect of PGI2 and PGE2
and their precursor, arachidonic acid, on the decrease in renal blood flow
elicited by renal nerve stimulation or by injected norepinephrine in
pentobarbital-anesthetized rats, with or without pretreatment with the
cyclooxygenase inhibitor, sodium meclofenamate. Administration of PGI2 or
PGE2 (0.4 micrograms X kg-1 X min-1) or arachidonic acid (5 micrograms X
kg-1 X min-1) into the renal artery reduced vascular resistance and
inhibited the vasoconstrictor response elicited by renal nerve stimulation
or by injected norepinephrine. In contrast, administration of sodium
meclofenamate (10 mg/kg iv + 30 micrograms X kg-1 X min-1) into the renal
artery increased renal vascular resistance and enhanced the renal
vasoconstrictor response to both adrenergic stimuli. In animals pretreated
with the cyclooxygenase inhibitor, the ability of arachidonic acid, but not
that of either PGE2 or PGI2, to reduce renal vascular resistance and the
vasoconstrictor response to either nerve stimulation or injected
norepinephrine was abolished. These data indicate that one or more
prostaglandins, probably PGE2 or PGI2, formed in the kidney reduce renal
vascular tone by their direct action on the vascular smooth muscle and by
attenuating the influence of adrenergic stimuli on renal vasculature.
