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Effect of prostaglandin inhibition on renin release comparison of furosemide and low sodium stimulation tests

, : Effect of prostaglandin inhibition on renin release comparison of furosemide and low sodium stimulation tests. Journal of Laboratory & Clinical Medicine 98(6): 929-937

Furosemide administration is considered comparable to Na restriction and upright posture as a stimulation test of PRA [plasma renin activity]. This view can be questioned if different mechanisms of renin release are involved. Prostaglandins appear to be an important mediator of renin release. Using a prostaglandin antagonist, indomethacin, the relative role of prostaglandins in the 2 renin stimulation tests was assessed. Eleven healthy volunteers on a high-Na intake had PRA and PA [plasma aldosterone] measured in response to furosemide stimulation before and during indomethacin administration and then in response to Na restriction combined with upright posture before and during indomethacin. Supine PRA was 0.41 ng/ml per h on high Na and 0.19 after indomethacin (P < 0.05). On low Na, the supine PRA was 2.07 ng/ml per h and 0.98 after indomethacin (P < 0.05). The increase in PRA (.DELTA.PRA) was 3.26 ng/ml per h with furosemide stimulation and 1.23 after indomethacin (P < 0.025). The PRA was 3.71 ng/ml per h with low-Na stimulation and upright posture and 2.53 after indomethacin (not significant). PA paralleled PRA except that there was no suppression of supine values with indomethacin. Prostaglandins apparently mediate baseline renin secretion and renin stimulation in response to furosemide. No comparable prostaglandin mediation could be demonstrated during renin stimulation secondary to Na restriction. The 2 standard renin stimulation tests appear to involve different mechanisms of renin release.

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