Effects of indomethacin on plasma renin activity in the conscious rat

The role of prostaglandins in the control of renin release in vivo was evaluated in the conscious rat. Indomethacin suppressed urinary prostaglandin E2 (PGE2) excretion from 5.3 +/- 0.5 to 2.6 +/- 0.5 ng/3 h (P less than 0.001). Basal plasma renin activity (PRA) fell from 6.20 +/- 1.07 to 2.98 +/- 0.45 ng . ml-1 . h-1 (P less than 0.02). Indomethacin suppressed PRA stimulated by furosemide, insulin-induced hypoglycemia, hydralazine, isoproterenol, arachidonic acid, and sodium-free diet, whereas PRA stimulated by PGE2 was not suppressed by indomethacin. The suppression of PRA by indomethacin in the sodium-deplete state rules out sodium retention as the mechanism of action of indomethacin. These results indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the renin response to several of the known stimulators, suggesting that prostaglandins may play a pivotal role in the control of renin release.