Circulation Research. 2002;90:18-20
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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© 2002 American Heart Association, Inc.
Reports |
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.
Correspondence to Prof Dr H. Nawrath, Pharmakologisches Institut, Universität Mainz, Obere Zahlbacher Str. 67, 55101 Mainz, Germany. E-mail Nawrath{at}mail.uni-mainz.de
Abstract
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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