| 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 |
Related Documents
:
|
18292183 - Probiotics ameliorate the hydrogen peroxide-induced epithelial barrier disruption by a ... 22425773 - Mechanisms involved in inhibition of chondrogenesis by activin-a. 14764533 - Pim-1 kinase inhibits stat5-dependent transcription via its interactions with socs1 and... |
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. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| 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
Previous Document: Extrarenal resistance to atrial natriuretic peptide in rats with experimental nephrotic syndrome.
Next Document: Nitroflurbiprofen, a new nonsteroidal anti-inflammatory, ameliorates structural injury in the remnan...