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- W2078996475 abstract "Concerning the letter by Kass and Takimoto (1) in PNAS regarding our recent publication (2), we would like to make the following comments. First, we agree that our results showing a “lack of importance” for cGMP-dependent protein kinase I (cGKI) as a modulator of cardiac hypertrophy only refers to the “basal” condition as we clearly stated in the manuscript (1, 2). We purposely did not use guanylyl cyclase stimulators or phosphodiesterase (PDE) inhibitors in these studies. However, we do note that, particularly under the stress conditions of isoproterenol infusion or aortic constriction, atrial natriuretic peptide is substantially increased. This provides substantial drive on cGMP synthesis. It is possible that cGKI needs to be induced by very high cGMP to have protective effects, although induction is not a requirement for the importance of this kinase in other tissues. The point here is that ablation of cGKI from cardiomyocytes and most other tissues (except vasculature) does not potentiate the ability of transverse aortic constriction (TAC) or isoproterenol (ISO) to cause hypertrophy. To us, this is an observation that needs to be reconciled with current dogma. The degrees of hypertrophy obtained in our studies were equal to or even higher than those obtained in many other studies." @default.
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- W2078996475 date "2010-05-24" @default.
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- W2078996475 title "Reply to Kass and Takimoto: Cardiac hypertrophy without cGKI and PDE5 in cardiac myocytes" @default.
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- W2078996475 doi "https://doi.org/10.1073/pnas.1005248107" @default.
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