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. Author manuscript; available in PMC: 2008 Jan 22.
Published in final edited form as: BJU Int. 2006 Oct 9;99(2):431–435. doi: 10.1111/j.1464-410X.2006.06577.x

FIG. 3.

FIG. 3

The proposed pathway by which sialorphin causes smooth muscle relaxation and thereby improves erectile function. CNP binds to its membrane receptor on corporal smooth muscle cells and activates GC-B. The CNP is degraded by NEP. However, in the presence of sialorphin (acting as a NEP inhibitor), the CNP has a prolonged effect, activating downstream mechanisms resulting in smooth muscle relaxation, mediated by the secondary messenger cGMP. Among these downstream activators are maxi-K channels. Efflux of potassium from the cells causes hyperpolarization of the smooth muscle cell membrane, inhibiting influx of Ca2+ through calcium channels. Lowered intracellular calcium causes inactivation myosin light-chain kinase (MLCK), thereby promoting smooth muscle relaxation. GTP, guanosine triphosphate, PKA, protein kinase A, PKC, protein kinase C; PKG, protein kinase G, MLC20, myosin light chain.