Role of the macula densa in renin release

Abstract

To examine the role of the macula densa in renin release, afferent arterioles alone or afferent arterioles with the macula densa attached were microdissected from rabbit kidney and incubated in Medium 199 for two consecutive 30-minute periods. Renin concentration in the medium was measured using partially purified rabbit angiotensinogen. Renin release rate over 1 hour from a single arteriole (or an arteriole with macula densa) was calculated and expressed as nanograms of angiotensin I generated per hour per arteriole (or arteriole with macula densa) per hour incubation (ngof ANG I, hr-1, Af-1/hour). Basal renin release rate from afferent arterioles was 0.69 ± 0.13ngof ANG I, hr-1, Af-1/hour (mean ± SEM, n = 9) and remained stable for 60 minutes. Basal renin release rate from arterioles with macula densa was 0.25 ± 0.03 ng of ANG I, hr-1, Af-1 MD-1/hour (n = 9), which was significantly lower (p < 0.025) than that from afferent arterioles alone. When furosemide (1.5 x 10-3 M) was added to afferent arterioles alone, no significant change in renin release was observed (percent change from control; 24.8 ± 29.9%; p > 0.05, n = 6). When furosemide was added to arterioles with macula densa attached, however, renin release increased by 387 ± 46% (n = 7; p < 0.001). After pretreatment with indomethacin, a cyclooxygenase inhibitor, furosemide still increased renin release from 0.17 ± 0.03 to 0.60 ± 0.10 ng of ANG I h r-1 Af+MD-1/hour(n = 4;p<0.05); however, indomethacin pretreatment reduced both the basal renin release rate and the absolute change in renin release induced by furosemide. We conclude that (1) the macula densa inhibits renin release in this preparation, (2) the macula densa plays a central role in furosemide-induced renin release, and (3) while the prostaglandin system is not essential for furosemide-induced renin release, it may be a modulating factor. © 1985 American Heart Association, Inc.