Document Detail

Vasopressin-stimulated prostaglandin E biosynthesis in the toad urinary bladder. Effect of water flow.
MedLine Citation:
PMID:  199620     Owner:  NLM     Status:  MEDLINE    
Prostaglandin E biosynthesis and its effect on water permeability were investigated in the toad urinary bladder. Arginine vasopressin (1 mU/ml) increased prostaglandin E (PGE) biosynthesis from 0.5+/-0.1 to 5.0+/-0.4 pmol/min per hemibladder (mean +/-SEM, n= 8, P less than 0.001). Maximal vasopressin-stimulated PGE biosynthesis, 6.4+/-0.2 pmol/min per hemibladder, occurred at vasopressin concentrations in excess of 3 mU/ml. Half-maximal stimulation of PGE biosynthesis occurred at a vasopressin concentration of approximately 0.7 mU/ml, whereas half-maximal stimulation of water flow occurred at a vasopressin concentration of approximately 5 mU/ml. Vasopressin-stimulated PGE biosynthesis did not depend on water flow along an osmotic gradient or upon sodium transport. Thin-layer chromatographic analysis of the lipids released from hemibladders labeled with tritium-arachidonic acid revealed that vasopressin stimulates the release of arachidonic acid from intracellular lipid stores without affecting the percentage of free arachidonic acid converted to PGE. Neither cyclic AMP nor theophylline stimulated PGE biosynthesis although they mimic arginine vasopressin (AVP) in stimulating water permeability. Biosynthesis of PGE was inhibited by mepacrine, a phospholipase inhibitor, and by agents that inhibit arachidonic acid oxygenase. The inhibition of PGE biosynthesis resulted in augmented vasopressin- and theophylline-stimulated water flow, but had no effect on cyclic AMP-stimulated water flow. We interpret these results to mean that endogenous PGE inhibits basal and vasopressin-stimulated adenylate cyclase activity. In contrast to the effects of AVP on permeability and transport, AVP stimulates PGE biosynthesis by a mechanism that does not depend on an increase in cellular cyclic AMP levels. The water permeability response of the toad urinary bladder to vasopressin is inhibited by PGE synthesized by the bladder in response to vasopressin.
R M Zusman; H R Keiser; J S Handler
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  60     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1977 Dec 
Date Detail:
Created Date:  1977-12-29     Completed Date:  1977-12-29     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1339-47     Citation Subset:  AIM; IM    
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MeSH Terms
Adenylate Cyclase / metabolism
Arachidonic Acids / metabolism
Arginine Vasopressin / pharmacology*
Chromatography, Thin Layer
Cyclic AMP / pharmacology
Lipid Metabolism
Prostaglandins E / biosynthesis*
Quinacrine / pharmacology
Stimulation, Chemical
Theophylline / pharmacology
Urinary Bladder / metabolism*
Vasopressins / analogs & derivatives*
Water / metabolism*
Reg. No./Substance:
0/Arachidonic Acids; 0/Prostaglandins E; 11000-17-2/Vasopressins; 113-79-1/Arginine Vasopressin; 58-55-9/Theophylline; 60-92-4/Cyclic AMP; 7732-18-5/Water; 83-89-6/Quinacrine; EC Cyclase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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