JPET xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Churchill, P. C.
Right arrow Articles by Churchill, M. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Churchill, P. C.
Right arrow Articles by Churchill, M. C.

Effects of trifluoperazine on renin secretion of rat kidney slices

PC Churchill and MC Churchill

It has been suggested recently that calmodulin acts as an intracellular "Ca-receptor," and that many Ca-dependent cellular activities are mediated in some manner by Ca-calmodulin. The renin-secretory activity of juxtaglomerular cells appears to be inversely related to intracellular Ca concentration (Ca); if Ca-calmodulin is the mediator in the secretory process, it follows that secretory rate should be inversely related to Ca-calmodulin activity. The purpose of these experiments was to determine the effects of trifluoperazine, an inactivator of Ca-calmodulin, on renin secretion of rat kidney slices. Over the range 10(-6) to 10(-4) M, trifluoperazine produced a concentration-dependent increase in renin release. As assessed by lactate dehydrogenase release, the trifluoperazine-induced increase in renin release cannot be attributed to increased cell membrane permeability to proteins. Thus, trifluoperazine stimulated renin secretion in a concentration-dependent manner. This is consistent with an inverse relation between Ca-calmodulin activity and renin secretion. However, in the presence of trifluoperazine, isoproterenol still stimulated and antidiuretic hormone, angiotensin II, high extracellular K concentration, ouabain and vanadate still inhibited renin secretion. Provided these stimulatory and inhibitory effects are associated with decreased and increased Ca, respectively, these observations are inconsistent with the hypothesis that the effects of Ca, on renin secretion are mediated by changes in Ca-calmodulin activity, since increases in Ca promote rather than attenuate the binding of trifluoperazine to calmodulin. It is concluded that trifluoperazine- stimulated renin secretion is mediated by a decrease in Cai produced by inhibition of Ca influx and/or stimulation of Ca efflux and/or sequestration.

Volume 224, Issue 1, pp. 68-72, 01/01/1983
Copyright © 1983 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
F. Schweda, G. A. J. Riegger, A. Kurtz, and B. K. Kramer
Store-operated calcium influx inhibits renin secretion
Am J Physiol Renal Physiol, July 1, 2000; 279(1): F170 - F176.
[Abstract] [Full Text] [PDF]

Home page
 J. Exp. Biol.Home page
A Kurtz and C Wagner
Cellular control of renin secretion
J. Exp. Biol., January 2, 1999; 202(3): 219 - 225.
[Abstract] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1983 by the American Society for Pharmacology and Experimental Therapeutics.