cGMP-Dependent Protein Kinase in the Regulation of Cardiovascular Functions

Cyclic GMP-dependent protein kinase (PKG) was discovered in 1970 in lobster muscle (Kuo & Greengard, 1970). It is a serine/threonine protein kinase specifically activated by cyclic guanosine monophosphate (cGMP). PKG is a ubiquitous intracellular second messenger mediating the biological effects of cGMP elevating agents including nitric oxide (NO), natriuretic peptides, and guanylin (an intestinal peptide involved in intestinal fluid regulation). It is now well recognized that PKG plays a central role in a broad range of physiological processes, such as contractility and proliferation of smooth muscle and cardiac myocytes, platelet aggregation, synaptic plasticity and learning, behavior, intestinal chloride reabsorption, renin secretion, and endochondral ossification (Francis et al., 2010; Hofmann et al., 2009; Lincoln et al., 2001; Lohmann & Walter, 2005). This chapter will focus on the role of PKG in the regulation of cardiovascular functions under physiological and pathophysiological conditions.