AJP - Regulatory, Integrative and Comparative Physiology, Vol 241, Issue 3 146-R151, Copyright © 1981 by American Physiological Society
Bradykinin effects on adrenergic transmission in the canine kidney: relation to prostaglandins
H. Susic, A. Nasjletti and K. U. Malik
We studied the action(s) of bradykinin at the renal vascular neuroeffector
junction, and its relation to prostaglandin synthesis, by investigating the
effect of the peptide on the renal venous output of the neurotransmitter
and on the renal vasoconstrictor responses elicited by sympathetic nerve
stimulation and by norepinephrine in pentobarbital-anesthetized dogs. Renal
arterial infusion of bradykinin at 10 ng . kg-1 . min-1 increased blood
flow to the kidney and inhibited the vasoconstrictor effect of renal nerve
stimulation (1-8 Hz) and injected norepinephrine (0.06-0.5 micrograms).
However, bradykinin did not alter the rise in venous output of
norepinephrine elicited by nerve stimulation. Infusion of another
vasodilatory peptide, substance P (2 ng . kg-1 . min-1) into the renal
artery also increased blood flow to the kidney but failed to alter the
vasoconstriction produced by either adrenergic stimulus. Pretreatment of
dogs with an inhibitor of prostaglandin synthesis, either sodium
meclofenamate or indomethacin (5 mg/kg), abolished the inhibitory effect of
the kinin on renal vasoconstriction produced by adrenergic stimuli. These
data suggest that bradykinin acts on postjunctional sites to reduce
adrenergically induced vasoconstriction in the canine kidney by a mechanism
dependent on prostaglandin synthesis.
