AJP - Renal Physiology, Vol 237, Issue 3 182-F187, Copyright © 1979 by American Physiological Society
Contribution of renal prostaglandins to the natriuretic action of bradykinin in the dog
M. C. Blasingham and A. Nasjletti
To study the effects of stimulation of renal prostaglandin biosynthesis by
bradykinin, we assessed the changes in renal functions induced by
intrarenal infusion of bradykinin (10 ng . min-1 . kg-1) in the dog
anesthetized with pentobarbital before and during inhibition of
prostaglandin synthesis by sodium meclofenamate (5 mg/kg). Before
meclofenamate administration, bradykinin augmented the urinary output of a
"PGE"-like substance from 1.00 +/- 0.25 to 3.88 +/- 1.09 ng/min (P less
than 0.05) and increased renal blood flow by 65 +/- 9 ml/min (P less than
0.001), urine flow by 0.55 +/- 0.23 ml/min (P less than 0.05), and sodium
excretion by 64.8 +/- 18.0 mueq/min (P less than 0.01). Administration of
meclofenamate did not affect the bradykinin-induced increase in renal blood
flow and urine volume, but suppressed the evoked output of "PGE" and
reduced the associated natriuresis, i.e., sodium excretion increased by
only 11.1 +/- 4.8 mueq/min (P greater than 0.05). In contrast,
meclofenamate did not affect the natriuresis effected by an equidilator
dose of PGE2 (5 ng . min-1 . kg-1) infused intrarenally. These observations
suggest that a product of prostaglandin synthetase produced by the kidney
during intrarenal infusion of bradykinin contributes to the natriuretic
action of the peptide.
