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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Circ Heart Fail. 2013 May;6(3):594–605. doi: 10.1161/CIRCHEARTFAILURE.112.000289

Figure 2. Simplified schematic of the natriuretic peptide system (NPS).

Figure 2

ANP, BNP and URO stimulate Cyclic GMP (cGMP) production by binding to the guanylyl cyclase (GC) receptor A, while CNP generates cGMP by binding to the GC-B receptor. Cyclic GMP modulates the activity of cGMP-dependent protein kinase G (PKG) to exert its pluripotent cardiac, vascular and renal biological actions. Cyclic GMP also regulates phosphodiesterases (PDEs) and cation channels. The cGMP signal is terminated by a variety of PDEs that hydrolyze cGMP to GMP. The NPs are removed from the circulation and inactived by the clearance receptor (NPR-C) and also degraded by a variety of peptidases including neprilysin (NEP) and dipeptidyl peptidase IV (DPPIV). In addition to the clearance capacity of NPR-C from the circulation, evidence has promoted the concept that the NPR-C mediates non-cGMP regulated biological actions.