In:
American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 277, No. 5 ( 1999-11-01), p. F706-F710
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
1931-857X
,
1522-1466
DOI:
10.1152/ajprenal.1999.277.5.F706
Language:
English
Publisher:
American Physiological Society
Publication Date:
1999
detail.hit.zdb_id:
1477287-5
