JPET Introducing ALZET?ew Model 2006 Pump

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


     

This Article
Right arrow Full Text
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
Right arrow Citation Map
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 Trachte, G. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Trachte, G. J.

Vol. 294, Issue 1, 210-215, July 2000

Depletion of Natriuretic Peptide C Receptors Eliminates Inhibitory Effects of C-Type Natriuretic Peptide on Evoked Neurotransmitter Efflux1

George J. Trachte

Department of Pharmacology, University of Minnesota-Duluth, School of Medicine, Duluth, Minnesota

Natriuretic peptides suppress evoked catecholamine efflux by a mechanism attributed to activation of the natriuretic peptide receptor (NPR)-C, but this designation relies on the absolute specificity of truncated natriuretic peptide analogs for the NPR-C. The NPR-C involvement in evoked catecholamine efflux was defined better in this study by selectively ablating the NPR-C in pheochromocytoma cells with antisense oligodeoxynucleotides. This treatment suppressed NPR-C levels by 52 ± 4% relative to missense treatment. The reduction of NPR-C levels suppressed evoked catecholamine efflux 33 ± 6% and eliminated the effect of C-type natriuretic peptide to suppress evoked catecholamine efflux. The native peptide, C-type natriuretic peptide, reduced evoked catecholamine efflux 39 ± 3% in cells with a normal complement of NPR-C. The NPR-C reduction failed to alter neuromodulatory effects of N-nitro-L-arginine methyl ester or an active fragment of the NPR-C receptor administered in permeabilized cells. Furthermore, the NPR-C reduction did not prevent guanylyl cyclase activation in response to C-type natriuretic peptide. These latter experiments indicate that the antisense treatment resulted in a specific suppression of the NPR-C and did not affect alternative neuromodulatory pathways or guanylyl cyclase receptors. The novel aspects of this study include both the inhibitory effect of NPR-C reduction on basal-evoked neurotransmitter efflux and the ablation of natriuretic peptide effects on neurotransmitter efflux by NPR-C reduction. The results are consistent with the notion of a key signal-transducing role of the NPR-C in mediating inhibitory effects of natriuretic peptides on neurotransmitter efflux.

1 This study was supported by U.S. Public Health Service Grant HL42525.

0022-3565/00/2941-0210$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2000 by The American Society for Pharmacology and Experimental Therapeutics


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
I. C. Villar, C. M. Panayiotou, A. Sheraz, M. Madhani, R. S. Scotland, M. Nobles, B. Kemp-Harper, A. Ahluwalia, and A. J. Hobbs
Definitive role for natriuretic peptide receptor-C in mediating the vasorelaxant activity of C-type natriuretic peptide and endothelium-derived hyperpolarising factor
Cardiovasc Res, June 1, 2007; 74(3): 515 - 525.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
L. R. Potter, S. Abbey-Hosch, and D. M. Dickey
Natriuretic Peptides, Their Receptors, and Cyclic Guanosine Monophosphate-Dependent Signaling Functions
Endocr. Rev., February 1, 2006; 27(1): 47 - 72.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. A. Rose, A. E. Lomax, and W. R. Giles
Inhibition of L-type Ca2+ current by C-type natriuretic peptide in bullfrog atrial myocytes: an NPR-C-mediated effect
Am J Physiol Heart Circ Physiol, December 1, 2003; 285(6): H2454 - H2462.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
G. J. Trachte
Natriuretic Peptides Suppress Protein Kinase C Activity to Reduce Evoked Dopamine Efflux from Pheochromocytoma (PC12) Cells
Endocrinology, January 1, 2003; 144(1): 94 - 100.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
S. E. Abbey and L. R. Potter
Lysophosphatidic Acid Inhibits C-Type Natriuretic Peptide Activation of Guanylyl Cyclase-B
Endocrinology, January 1, 2003; 144(1): 240 - 246.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
P. M. Bryan and L. R. Potter
The Atrial Natriuretic Peptide Receptor (NPR-A/GC-A) Is Dephosphorylated by Distinct Microcystin-sensitive and Magnesium-dependent Protein Phosphatases
J. Biol. Chem., May 3, 2002; 277(18): 16041 - 16047.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
X.-l. He, D.-c. Chow, M. M. Martick, and K. Christopher Garcia
Allosteric Activation of a Spring-Loaded Natriuretic Peptide Receptor Dimer by Hormone
Science, August 31, 2001; 293(5535): 1657 - 1662.
[Abstract] [Full Text] [PDF]


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

Copyright © 2000 by the American Society for Pharmacology and Experimental Therapeutics.