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(Circulation Research. 2004;94:e55.)
© 2004 American Heart Association, Inc.

Letter to the Editor

The Janus Faces of NO?

Axel Gödecke, Jürgen Schrader

Institut für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany, Axel.Goedecke@uni-duesseldorf.de

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

The functional effects of myocardial iNOS expression are still a matter of controversy.¹ To directly address the role of iNOS on myocardial function, two transgenic animal models with cardiac-specific overexpression of iNOS have been generated.^2,3 Mungrue et al describe the generation and analysis of a binary transgenic mouse model for a tetracycline-inducible, cardiac-specific expression of iNOS (tTA-iNOS mice). The authors find higher mortality after induction of iNOS expression and link this phenotype to disturbances of the cardiac conductance. The results are in contrast with another report on the effects of chronic overexpression of iNOS in the heart of transgenic mice under the control of the -MHC promoter (tg-iNOS mice), which was published in this journal.² These latter mice show only minimal alterations of cardiac function measured in vivo and ex vivo and no signs of higher mortality or sudden death.

Mungrue and coworkers addressed the differences between both models already in an earlier publication and concluded that Heger et al did not analyze myocardial overexpression of iNOS but rather selected for mice with inactive iNOS. To support this view, Mungrue et al claim that Heger et al did not conclusively show that iNOS was active in transgenic hearts in vivo and suspected that the iNOS activity in their conditional model was higher than in the constitutive model.³ This unproven assumption was extended by further unassigned speculations in a Letter to the Editor published in Circulation Research,⁴ in which Mungrue et al respond to a recent publication . . . [Full Text of this Article]

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