Effect of A Renal Prostaglandin on Distribution of Blood Flow in the Isolated Canine Kidney
In isolated blood-perfused canine kidneys, progressive increases in renal blood flow and its fractional distribution to the inner cortex were correlated with increases in perfusate concentrations of a prostaglandin E-like (PGE-like) substance. The ratio of blood flow to the outer and inner halves of the renal cortex measured by the radioactive-microsphere method changed from 77:23 to 68:32 (P < 0.001) after 90 minutes of perfusion; simultaneously, the concentration of the PGE-like substance increased from 0.04 ng/ml to 0.59 ng/ml (P < 0.02). Thus, the greatest rate of increase in the concentration of the PGE-like substance occurred coincidently with the largest increase in inner cortical blood flow, i.e., from 30 ml/min to 69 ml/min (P < 0.001). During the two subsequent 90-minute perfusion periods, the ratio of outer cortical blood flow to inner cortical blood flow fell to 61:39, and the concentration of the PGE-like substance increased further. When indomethacin was added to the perfusate, the concentration of the PGE-like substance decreased from 1.00 ng/ml to 0.24 ng/ml (P < 0.05), and renal blood flow decreased, especially in the inner cortex where the decline was from 34% to 19% of total renal blood flow (P < 0.05). Thus, renal blood flow was redistributed after indomethacin was administered. PGE2 was infused to determine whether substitution for the loss of circulating PGE-like substance could prevent the effects of indomethacin on the distribution of renal blood flow. Despite administration of exogenous PGE2, renal blood flow redistributed after administration of indomethacin, and the ratio of outer cortical blood flow to inner cortical blood flow increased from 68:32 to 80:20 (P < 0.05). These results suggest that the intrarenal site of synthesis and release of PGE2 determines its action as a local hormone affecting deep cortical blood flow.
- prostaglandin E2
- local hormones
- renal inner cortical blood flow
- regulation of the renal circulation
- antiinflammatory compounds
- inhibition of prostaglandin synthetase
- renal hormones
- Received August 13, 1973.
- Accepted March 13, 1974.
- © 1974 American Heart Association, Inc.