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Cyclic nucleotide signaling in cavernous smooth muscle
Ching-Shwun Lin1, Guiting Lin, Tom F Lue
1Knuppe Molecular Urology Laboratory, Department of Urology, University of California, San Francisco, CA 94143-1695, USA. clin@urol.ucsf.edu
The Journal of Sexual Medicine
|January 21, 2006
Summary
Nitric oxide (NO) triggers sexual erection via the NO/sGC/cGMP/PKG pathway. Erectile dysfunction can involve alterations in cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) pathways, offering therapeutic targets.
Area of Science:
- Physiology
- Biochemistry
- Pharmacology
Background:
- Penile erection relies on smooth muscle relaxation, primarily regulated by cyclic nucleotide signaling.
- Understanding these pathways is crucial for scientists and clinicians studying erectile function and dysfunction.
Purpose of the Study:
- To review the roles of signaling molecules, receptors, effectors, and phosphodiesterases in cyclic nucleotide signaling for smooth muscle relaxation.
- To discuss the involvement of these pathways in erectile dysfunction and their therapeutic potential.
Main Methods:
- A comprehensive literature search was conducted using Entrez with keywords related to vascular, cavernous, smooth muscle, signaling molecules, and cyclic nucleotide pathways.
- Publications specifically on erectile function/dysfunction were prioritized.
Main Results:
- Both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) pathways are identified in cavernous smooth muscle.
- Nitric oxide (NO) is the key molecule for sexually induced erection, signaling through soluble guanyl cyclase (sGC), cGMP, and protein kinase G (PKG).
Conclusions:
- The NO/sGC/cGMP/PKG pathway is central to sexually stimulated erection.
- Phosphodiesterase 5 (PDE5) mediates detumescence by degrading cGMP.
- Alterations in cAMP and cGMP pathways are linked to erectile dysfunction, presenting potential therapeutic targets.