Circulation Research. 2001
Published online before print December 6, 2001, doi: 10.1161/hh0102.103222
Published online before print December 6, 2001, doi: 10.1161/hh0102.103222
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Submitted on October 4, 2001
Revised on November 26, 2001
Accepted on November 26, 2001
cGMP-Dependent Protein Kinase I Mediates the Negative Inotropic Effect of cGMP in the Murine Myocardium
From the Pharmakologisches Institut (J.W.W., H.N.), Universität Mainz, Germany; Institut für Pharmakologie und Toxikologie (W.W., S.K., C.W., F.H., R.F.), Technische Universität München, Germany.
* To whom correspondence should be addressed. E-mail: Nawrath{at}mail.uni-mainz.de.
To study the role of cGMP-dependent protein kinase I (cGKI) for cardiac contractility, force of contraction (Fc) was studied in electrically driven heart muscle from wild-type (WT) mice and from conventional and conditional cGKI knockout mice. Both 8-Br-cGMP and 8-pCPT-cGMP reduced Fc in cardiac muscle from juvenile WT but not from juvenile cGKI-null mutants. Similarly, the cGMP analogues reduced Fc in forskolin-stimulated ventricular muscle from WT mice but not from cGKI-null mutants. In contrast, carbachol reduced Fc in both groups of animals. 8-Br-cGMP reduced Fc also in heart muscle from adult WT mice but not from adult cardiomyocyte-specific cGKI-knockout mice. These results demonstrate that cGKI mediates the negative inotropic effect of cGMP in the myocardium of juvenile and adult mice.
Key words: contractility • mouse • gene targeting • Cre recombinase
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