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Nitric oxide (NO) acts as essential regulator of vasculogenesis and angiogenesis and is critical for arteriogenesis. Whether NO’s effects in vivo are mediated through NO-sensitive guanylyl cyclase (NO-GC) and thus by cGMP-dependent mechanisms has been only poorly addressed. Mice lacking NO-GC globally or specifically in smooth muscle cells (SMC) or(More)
NO-sensitive guanylyl cyclase (NO-GC) is accepted to be the major receptor for the signaling molecule NO. Deletion of NO-GC in mice leads to disturbed NO/cGMP signaling. As a result, these mice show abolished NO-dependent relaxation of smooth muscle-containing tissues in the cardiovascular and gastrointestinal systems. Mice with general deletion suffer from(More)
Phosphodiesterases (PDE) are considered to be key players in many signal transduction pathways. They degrade the second messengers cGMP and cAMP, thereby controlling their intracellular levels. So far, eleven PDE families, typically having several isoforms and splice variants are known. The PDE10 family is encoded by one gene that gives rise to at least two(More)
The second messenger cGMP is involved in several physiological functions such as smooth muscle relaxation and inhibition of platelet aggregation. Besides cGMP synthesis , hydrolysis of cGMP by cyclic nucleotide phosphodi-esterases (PDEs) determines the shape of cGMP signals. Eleven PDE families are known differing in regulation and cAMP/cGMP specificity.(More)
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