The effect of prostaglandin inhibition on renin release. A comparison of furosemide and low-sodium stimulation tests

Furosemide administration is considered comparable to sodium restriction and upright posture as a stimulation test of PRA. 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, we attempted to assess the relative role of prostaglandins in the two renin stimulation tests. Eleven healthy volunteers on a high-sodium intake had PRA and PA measured in response to furosemide stimulation before and during indomethacin administration and then in response to sodium restriction combined with upright posture before and during indomethacin. Supine PRA was 0.41 ng/ml/hr on high sodium and 0.19 after indomethacin (p < 0.05). On low sodium, the supine PRA was 2.07 ng/ml/hr and 0.98 after indomethacin (p < 0.05). The increase in PRA (ΔPRA) was 3.26 ng/ml/hr with furosemide stimulation and 1.23 after indomethacin (p < 0.025). The PRA was 3.71 ng/ml/hr with low-sodium stimulation and upright posture and 2.53 after indomethacin (NS). PA paralleled PRA except that there was no suppression of supine values with indomethacin. We conclude that prostaglandins mediate baseline renin secretion and renin stimulation in response to furosemide. However, no comparable prostaglandin mediation could be demonstrated during renin stimulation secondary to sodium restriction. The two standard renin stimulation tests appear to involve different mechanisms of renin release.