JPET

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 McCarthy, K. D.
Right arrow Articles by Reed, D. J
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McCarthy, K. D.
Right arrow Articles by Reed, D. J
Journal of Pharmacology And Experimental Therapeutics, Vol. 189, Issue 1, 194-201, 1974
Copyright © 1974 by American Society for Pharmacology and Experimental Therapeutics

THE EFFECT OF ACETAZOLAMIDE AND FUROSEMIDE ON CEREBROSPINAL FLUID PRODUCTION AND CHOROID PLEXUS CARBONIC ANHYDRASE ACTIVITY

Ken D. McCarthy 1 and Donal J Reed 1

1 Department of Pharmacology, University of Utah College of Medicine, Salt Lake City, Utah

The ability of acetazolamide and furosemide to inhibit cerebrospinal fluid (CSF) flow and choroid plexus carbonic anhydrase was measured in adult New Zealand White rabbits of either sex. CSF formation rates were measured by the inulin-dilution technique and carbonic anhydrase activity by the changing-pH method. The maximal reduction in CSF flow with either drug was between 50 and 60%. Acetazolamide did not decrease CSF flow rate until over 99.5% of choroid plexus carbonic anhydrase was inhibited. In contrast, furosemide caused a significant decrease in CSF flow with less than 98% inhibition of choroid plexus carbonic anhydrase. In vitro studies showed that acetazolamide is about 100 times as potent as furosemide in the inhibition of carbonic anhydrase of the choroid plexus. Based on the assumption that the decrease in CSF flow with acetazolamide is due solely to carbonic anhydrase inhibition, then furosemide must be acting, at least partially, by a mechanism other than the inhibition of choroid plexus carbonic anhydrase. If acetazolamide and furosemide decrease flow by different mechanisms, the effects of the two drugs may be additive with respect to inhibition of CSF flow and it may be possible to reduce CSF flow more than the approximately 50% that can be accomplished with the individual therapeutic agents presently in use.

Submitted on June 25, 1973
Accepted on December 17, 1973




This article has been cited by other articles:


Home page
 EDUCATION AND PRACTICEHome page
Y Y Matthews
Drugs used in childhood idiopathic or benign intracranial hypertension
Arch. Dis. Child. Ed. Pract., February 1, 2008; 93(1): 19 - 25.
[Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
I. Bergman, G. J. Burckart, C. R. Pohl, R. Venkataramanan, M. A. Barmada, J. A. Griffin, and N.-K. V. Cheung
Pharmacokinetics of IgG and IgM Anti-Ganglioside Antibodies in Rats and Monkeys after Intrathecal Administration
J. Pharmacol. Exp. Ther., January 1, 1998; 284(1): 111 - 115.
[Abstract] [Full Text]

Home page
 J Child NeurolHome page
J. F. Schoeman
Childhood Pseudotumor Cerebri: Clinical and Intracranial Pressure Response to Acetazolamide and Furosemide Treatment in a Case Series
J Child Neurol, April 1, 1994; 9(2): 130 - 134.
[Abstract] [PDF]


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

Copyright © 1974 by the American Society for Pharmacology and Experimental Therapeutics.