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Editorial
. 2016 Dec;112(3):619-621.
doi: 10.1093/cvr/cvw225. Epub 2016 Oct 23.

Natriuretic peptides and peripheral autonomic neurotransmission: back to the A, B, and C's

Olujimi A Ajijola  1 , Kalyanam Shivkumar  1 , Beth A Habecker  2
Affiliations
Editorial

Natriuretic peptides and peripheral autonomic neurotransmission: back to the A, B, and C's

Olujimi A Ajijola et al. Cardiovasc Res. 2016 Dec.
No abstract available

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Figures

Figure 1
Figure 1
Simplified schematic illustrating the intracellular signalling cascade potentially utilized by B-type and C-type natriuretic peptide (BNP and CNP, respectively) and their corresponding natriuretic peptide receptors (NPR) A and B. Binding of NP-NPR binding activates particulate guanylyl cyclase (pGC), producing cylic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP) as a result. cGMP activates protein kinase G (PKG, also known as cGMP-activated protein kinase). PKG inhibits calcium influx via voltage gated calcium channels (VGCC), which are activated upon neuronal depolarization. When phosphodiesterase 2 levels are elevated (as seen in chronic sympathoexcitation e.g., spontaneously hypertensive rat), the ability of BNP, and possibly CNP to reduce neurotransmitter release is diminished due to PDE2-mediated degradation of cGMP into 5’GMP.
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References

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