Volume 11 Supplement 1

5th International Conference on cGMP: Generators, Effectors and Therapeutic Implications

Open Access

cGMP signals in smooth muscle cells and cardiac myocytes

  • Christian Krawutschke1Email author,
  • Doris Koesling1 and
  • Michael Russwurm1
BMC Pharmacology201111(Suppl 1):P40

https://doi.org/10.1186/1471-2210-11-S1-P40

Published: 1 August 2011

Background

cGMP plays an important role in the cardiovascular system and is involved in smooth muscle relaxation and inhibition of platelet aggregation. cGMP concentrations inside cells are determined by an interplay of cGMP synthesis through natriuretic peptide or NO receptor guanylyl cyclases on the one hand and cGMP-degrading phosphodiesterases on the other hand.

Phosphodiesterase 5 has been suggested to play a role in cGMP hydrolysis in cardiac myocytes. Strong antihypertrophic effects of PDE5 inhibition by sildenafil have been observed in animal models and clinical trials have been started to approve sildenafil for the treatment of cardiac hypertrophy.

Nevertheless, cGMP increases induced by nitric oxide or natriuretic peptides in cardiac myocytes remain difficult to assess. Currently, cGMP levels are measured by radioimmunoassays (RIA) or enzyme-linked immunosorbent assays (ELISA) using cGMP-specific antibodies. Although femtomolar amounts of cGMP can be detected, relatively high agonist concentrations are required to obtain measurable cGMP increases.

Results

Here, we measured cGMP elevations by fluorescence resonance energy transfer (FRET)-based cGMP indicators to compare cGMP signals in cardiac myocytes and smooth muscle cells.

Authors’ Affiliations

(1)
Institut für Pharmakologie und Toxikologie, Medizinische Fakultät, Ruhr-Universität Bochum

Copyright

© Krawutschke et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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