AJP - Renal Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol 249: F739-F744, 1985;
0363-6127/85 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Filep, J.
Right arrow Articles by Frolich, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Filep, J.
Right arrow Articles by Frolich, J. C.

AJP - Renal Physiology, Vol 249, Issue 5 739-F744, Copyright © 1985 by American Physiological Society


ARTICLES

Vascular and renal effects of leukotriene C4 in conscious rats

J. Filep, B. Rigter and J. C. Frolich

To investigate the possible renal effects of leukotriene C4 (LTC4) renal function was monitored in conscious unrestrained rats. Intravenous injections of 2, 4, and 8 micrograms/kg LTC4 markedly and dose-dependently elevated urine flow (by 64, 91, and 133%, respectively) with a concomitant increase in urinary sodium (61, 81, and 118%) and potassium (39, 50, and 76%) excretion. All changes were statistically significant. There was a tendency for glomerular filtration rate to increase, but this change reached statistical significance only after the highest dose of LTC4. Moreover, 8 micrograms/kg LTC4 reduced p-aminohippurate clearance by 33%. A dose-dependent increase in mean arterial pressure (15 mmHg at 2 micrograms/kg, 20 mmHg at 4 micrograms/kg, and 30 mmHg at 8 micrograms/kg) was observed following LTC4 administration. While the administration of FPL 55712, a putative antagonist of leukotrienes, had no effect on mean arterial pressure and kidney function, it significantly attenuated the vasopressor effect of LTC4 and practically completely abolished LTC4-induced changes in both renal hemodynamics and water and electrolyte excretion. These results raise the possibility that leukotrienes might be involved in the regulation of renal hemodynamics and could modify urinary electrolyte excretion under conditions in which leukotriene formation is enhanced.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online