ArticleInternational journal of impotence research
Role of the soluble guanylyl cyclase alpha1-subunit in mice corpus cavernosum smooth muscle relaxation.
Article in International journal of impotence research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Stimulators and activators of soluble guanylate cyclase for urogenital disorders.Nature reviews. Urology · 2018Review
- Riociguat: a soluble guanylate cyclase stimulator for the treatment of pulmonary hypertension.Drug design, development and therapy · 2017Review
- Gas what: NO is not the only answer to sexual function.British journal of pharmacology · 2015Review
- Cyclic guanosine monophosphate and the dependent protein kinase regulate lymphatic contractility in rat thoracic duct.The Journal of physiology · 2013Article
- Preserved fertility despite erectile dysfunction in mice lacking the nitric oxide receptor.The Journal of physiology · 2013Article
- In vitro and in vivo studies on the importance of the soluble guanylyl cyclase α1 subunit in penile erection.World journal of urology · 2010Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Soluble guanylyl cyclase (sGC) is the major effector molecule for nitric oxide (NO) and as such an interesting therapeutic target for the treatment of erectile dysfunction. To assess the functional importance of the sGCalpha(1)beta(1) isoform in corpus cavernosum (CC) relaxation, CC from male sGCalpha(1)(-/-) and wild-type mice were mounted in organ baths for isometric tension recording. The relaxation to endogenous NO (from acetylcholine, bradykinin and electrical field stimulation) was nearly abolished in the sGCalpha(1)(-/-) CC. In the sGCalpha(1)(-/-) mice, the relaxing influence of exogenous NO (from sodium nitroprusside and NO gas), BAY 41-2272 (NO-independent sGC stimulator) and T-1032 (phosphodiesterase type 5 inhibitor) were also significantly decreased. The remaining exogenous NO-induced relaxation seen in the sGCalpha(1)(-/-) mice was significantly decreased by the sGC-inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one. The specificity of the impairment of the sGC-related responses was demonstrated by the unaltered relaxations seen with forskolin (adenylyl cyclase activator) and 8-pCPT-cGMP (cGMP analog). In conclusion, the sGCalpha(1)beta(1) isoform is involved in corporal smooth muscle relaxation in response to NO and NO-independent sGC stimulators. The fact that there is still some effect of exogenous NO in the sGCalpha(1)(-/- mice suggests the contribution of (an) additional pathway(s).
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