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J. Biol. Chem., Vol. 277, Issue 45, 42423-42430, November 8, 2002
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From the Department of Biochemistry, Molecular Biology, and
Biophysics, University of Minnesota, Minneapolis, Minnesota
55455
Natriuretic peptides bind their
cognate cell surface guanylyl cyclase receptors and elevate
intracellular cGMP concentrations. In vascular smooth muscle cells,
this results in the activation of the type I cGMP-dependent
protein kinase and vasorelaxation. In contrast, pressor hormones like
arginine-vasopressin, angiotensin II, and endothelin bind serpentine
receptors that interact with Gq and activate
phospholipase C
Vasopressin-dependent Inhibition of the C-type
Natriuretic Peptide Receptor, NPR-B/GC-B, Requires Elevated
Intracellular Calcium Concentrations*
and
. The products of this enzyme, diacylglycerol and
inositol trisphosphate, activate the conventional and novel forms of
protein kinase C (PKC) and elevate intracellular calcium
concentrations, respectively. The latter response results in
vasoconstriction, which opposes the actions of natriuretic peptides.
Previous reports have shown that pressor hormones inhibit natriuretic
peptide receptors NPR-A or NPR-B in a variety of different cell types.
Although the mechanism for this inhibition remains unknown, it has been
universally accepted that PKC is an obligatory component of this
pathway primarily because pharmacologic activators of PKC mimic the
inhibitory effects of these hormones. Here, we show that in A10
vascular smooth muscle cells, neither chronic PKC down-regulation nor
specific PKC inhibitors block the AVP-dependent desensitization of NPR-B even though both processes block
PKC-dependent desensitization. In contrast, the
cell-permeable calcium chelator, BAPTA-AM
(1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, tetraacetoxymethyl ester), abrogates the
AVP-dependent desensitization of NPR-B, and ionomycin, a
calcium ionophore, mimics the AVP effect. These data show that the
inositol trisphosphate/calcium arm of the phospholipase C pathway
mediates the desensitization of a natriuretic peptide receptor in A10
cells. In addition, we report that CNP attenuates
AVP-dependent elevations in intracellular calcium
concentrations. Together, these data reveal a dominant role for
intracellular calcium in the reciprocal regulation of these two
important vasoactive signaling systems.
*
Scientist Development Award 0130398 from the National
Division of the American Heart Association, National Institutes of
Health Grant RO1HL66397, and a grant from the Minnesota Medical
Foundation (all to L. R. P.) provided financial support for these
studies.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported in part by National Institutes of Health Training Grant AR07612.
§
To whom correspondence should be addressed: Dept. of Biochemistry,
Molecular Biology, and Biophysics, University of Minnesota, 6-155 Jackson, 321 Church St., S. E., Minneapolis, MN 55455. Tel.: 612-624-7251; Fax: 612-624-7282; E-mail: potter@umn.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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