Document Detail


Phosphoinositide signaling in rat inner medullary collecting duct.
MedLine Citation:
PMID:  9530273     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous studies in microdissected rat inner medullary collecting duct (IMCD) segments have demonstrated that carbachol, arginine vasopressin (AVP), and the V2 vasopressin receptor agonist 1-desamino-8-D-arginine vasopressin (DDAVP) induce a similar increase in intracellular Ca2+. The present study tested whether these agents activate the phosphoinositide hydrolysis pathway. In intracellular inositol 1,4,5-trisphosphate (IP3) measurements, we found that IMCD suspensions incubated with AVP or DDAVP (10(-8) M) displayed no measurable increase in IP3, whereas IMCD suspensions incubated with the muscarinic cholinergic agent carbachol (100 microM) induced a significant increase in IP3 production. Similarly, carbachol, but not AVP or DDAVP, induced a significant increase in membrane-associated protein kinase C (PKC) enzyme activity. To test what specific PKC isoforms are activated by carbachol in IMCD, we first characterized the PKC isoforms in IMCD suspensions by immunoblotting using affinity-purified antibodies against different PKC isoforms. We identified one classic PKC isoform (alpha), three novel PKC isoforms (delta, epsilon, eta), and one atypical PKC isoform (zeta) in the IMCD. Carbachol induced a cytosol-to-membrane translocation of the PKC-eta isoform but did not alter the distribution of any other isoform. In contrast, AVP had no effect on the distribution of any PKC isoform tested. These data, taken together, demonstrate that carbachol is an activator of the phosphoinositide hydrolysis pathway in IMCD but do not demonstrate signaling via this pathway in response to AVP or DDAVP. These results suggest that the previously observed AVP-stimulated Ca2+ mobilization in IMCD may be due to a mechanism other than activation of the phosphoinositide hydrolysis pathway.
Authors:
C L Chou; S I Rapko; M A Knepper
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The American journal of physiology     Volume:  274     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1998 Mar 
Date Detail:
Created Date:  1998-04-14     Completed Date:  1998-04-14     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  F564-72     Citation Subset:  IM    
Affiliation:
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arginine Vasopressin / pharmacology*
Carbachol / pharmacology*
Cell Compartmentation / drug effects
Cell Membrane / enzymology
Cytosol / enzymology
Deamino Arginine Vasopressin / pharmacology*
Immunologic Techniques
Isoenzymes / physiology
Kidney Medulla / physiology*
Kidney Tubules, Collecting / physiology*
Phosphatidylinositols / physiology*
Protein Kinase C / physiology*
Rats
Rats, Sprague-Dawley
Receptors, Vasopressin / agonists
Signal Transduction / drug effects
Chemical
Reg. No./Substance:
0/Isoenzymes; 0/Phosphatidylinositols; 0/Receptors, Vasopressin; 113-79-1/Arginine Vasopressin; 16679-58-6/Deamino Arginine Vasopressin; 51-83-2/Carbachol; EC 2.7.11.13/Protein Kinase C

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


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