Skip to main content
  • Poster presentation
  • Open access
  • Published:

ATP-independent activation of natriuretic peptide receptors

Natriuretic peptide receptor A (NPR-A) is an essential cardiovascular regulator that is stimulated by atrial natriuretic peptide and brain natriuretic peptide, whereas natriuretic peptide receptor B (NPR-B) stimulates long bone growth in a C-type natriuretic peptide-dependent manner. Many reports indicate that ATP is essential for NPR-A and NPR-B activation. Current models suggest that natriuretic peptide binding to receptor extracellular domains causes ATP binding to intracellular kinase homology domains, which derepresses adjacent catalytic domains. Here, we report 100-fold activation of natriuretic peptide receptors in the absence of ATP. Addition of a nonhydrolyzable ATP analog had no effect at early time periods (seconds) but increased cGMP production about two-fold after longer incubations (minutes), consistent with a stabilization, not activation, mechanism. These data indicate that ATP does not activate natriuretic peptide receptors. Instead, ATP increases activity primarily by maintaining proper receptor phosphorylation status, but also serves a previously unappreciated enzyme stabilizing function.

Author information

Authors and Affiliations


Corresponding author

Correspondence to Lincoln R Potter.

Rights and permissions

Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and permissions

About this article

Cite this article

Antos, L.K., Abbey-Hosch, S.E., Flora, D.R. et al. ATP-independent activation of natriuretic peptide receptors. BMC Pharmacol 5 (Suppl 1), P3 (2005).

Download citation

  • Published:

  • DOI: