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Atrial Natriuretic Peptide Suppresses the Transcription of Its Guanylyl Cyclase-linked Receptor (*)

L. Cao,Jianming Wu,D. Gardner

Published 1995 in Journal of Biological Chemistry

ABSTRACT

Atrial natriuretic peptide (ANP) treatment of rat aortic smooth muscle cells suppressed both I-ANP binding and ANP-dependent cGMP accumulation, suggesting reductions in the type C (NPR-C) and type A (NPR-A) natriuretic peptide receptor populations, respectively. NPR-A, but not NPR-C, mRNA levels were reduced in a dose-dependent fashion by ANP. The latter effect appeared to be due, at least in part, to suppression of NPR-A gene promoter activity. ANP effected a dose- and time-dependent reduction in a transiently transfected NPR-A luciferase reporter (−1575LUC). Analysis of 5′ deletion mutants of the NPR-A promoter demonstrated that the ANP-dependent sequence lies between −1575 and −1290 relative to the transcription start site. Inhibition of the ANP promoter was also effected by brain natriuretic peptide, type C natriuretic peptide, and 8-bromo-cGMP, but not by the NPR-C-selective ligand cANF. In the case of 8-bromo-cGMP, the responsive element(s) was localized to the same 285-base pair region linked to the ANP effect above. These findings indicate that ANP autoregulates its own receptors in these cells and, at least in the case of NPR-A, it does so through suppression of receptor gene expression and receptor synthesis. This suppression may operate through a cGMP-dependent element located more than a kilobase upstream from the transcription start site.

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