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Am J Physiol Renal Physiol 277: F706-F710, 1999;
0363-6127/99 $5.00
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Vol. 277, Issue 5, F706-F710, November 1999

Inhibition of macula densa-stimulated renin secretion by pharmacological blockade of cyclooxygenase-2

Timothy R. Traynor, Ann Smart, Josephine P. Briggs, and Jurgen Schnermann

University of Michigan Medical School, Department of Physiology, Ann Arbor, Michigan 48109, and National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892

Previous results from our laboratory have shown that in the isolated perfused juxtaglomerular apparatus, nonselective inhibitors of cyclooxygenase (COX) activity prevent the stimulation of renin secretion by a reduction in luminal NaCl concentration at the macula densa. The present studies were performed to examine which COX isoform is involved in NaCl-dependent renin secretion. In the absence of COX inhibitors, a reduction in luminal NaCl (from Na 141/Cl 120 mM to Na 26/Cl 7 mM) caused an increase in renin secretion rate from 4.5 ± 1.8 to 26.1 ± 7.4 nGU/min (P < 0.01, n = 19). The presence of the COX-1 inhibitor valerylsalicylate (500 µM) in lumen and bath did not affect the stimulation of renin secretion by a reduction in luminal NaCl concentration (5 ± 1.8 nGU/min at high NaCl, and 30.5 ± 9.4 nGU/min at low NaCl; P < 0.01, n = 8). In contrast, the specific COX-2 inhibitor NS-398 (50 µM) in lumen and bath abolished the stimulating effect of low luminal NaCl (12.8 ± 3.9 nGU/min at high NaCl, and 10.7 ± 3.1 nGU/min at low NaCl; NS, n = 15). The finding that COX-2 is critically involved in macula densa control of renin secretion indicates that the COX-2-expressing epithelial cells in the tubuloglomerular contact area are a likely source of prostaglandins participating in the signaling pathway between the macula densa and renin-producing granular cells.

kidney; rabbit; NS-398; valerylsalicylate; isolated perfused juxtaglomerular apparatus


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