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Background In many tissues, a key mediator of cGMP signaling is cGMP-dependent protein kinase I (PKG I). In vitro and in vivo studies have shown that cGMP may not only regulate the kinase activity but also the expression levels of PKG I. Thus, chronic exposure of smooth muscle cells to high levels of NO or NO donors, via increased cellular cGMP, suppresses PKG I expression, which may partly explain the phenomenon of NO and/or nitrate tolerance. However, it is not known whether the opposite situation, namely a reduction in cellular cGMP levels, can increase PKG I expression. To investigate this question, we examined the expression and activity of PKG I in different tissues of mice with genetic deletion of guanylyl cyclase-A (GC-A KO), an in vivo model of reduced cGMP formation in many different cell types.

Increased tissue expression and activity of cGMP-dependent protein kinase I in ANP-receptor (GC-A) – deficient mice