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Title: Hydrogen sulfide promotes nitric oxide production in corpus cavernosum by enhancing expression of endothelial nitric oxide synthase
Authors: Meng, J. 
Adaikan, P.G. 
Srilatha, B. 
Keywords: erectile dysfunction
hydrogen sulfide
nitric oxide
nitric oxide synthase
Issue Date: May-2013
Citation: Meng, J., Adaikan, P.G., Srilatha, B. (2013-05). Hydrogen sulfide promotes nitric oxide production in corpus cavernosum by enhancing expression of endothelial nitric oxide synthase. International Journal of Impotence Research 25 (3) : 86-90. ScholarBank@NUS Repository.
Abstract: Recently, hydrogen sulfide (H 2 S) has been identified as a potential therapy for ED. However, a thorough understanding of its molecular mechanisms of action would be essential to develop H 2 S as a new therapy for ED. In this study, the effect of H 2 S on nitric oxide (NO) production, especially through the expression of constitutive nitric oxide synthase (NOS) isoforms - endothelial NOS (eNOS) and neuronal NOS (nNOS) in rat corpus cavernosum (CC) were explored. Real-time PCR studies subsequent to in vitro treatment of sodium hydrosulfide hydrate (NaHS), a stable H 2 S donor, showed increases in eNOS but not nNOS mRNA. Western blot studies confirmed that the exogenously applied NaHS increased eNOS but not nNOS protein expression in the rat CC. Furthermore, NaHS did not alter the expressed amounts of Caveolin-1 (CAV-1), a dominant inhibitory interaction partner of eNOS, in these tissues. Not surprisingly, NaHS also enhanced the NO production in eNOS-associated membrane fraction of rat CC. Taken together, we ascertain that H 2 S could exert its proerectile effects by augmenting NO pathway. It appears that H 2 S would be particularly useful in improving the clinical outcome of ED patients, whose erectile impairment is due to an inherent attenuation of the endothelial NO formation in the cavernosum. © 2012 Macmillan Publishers Limited All rights reserved.
Source Title: International Journal of Impotence Research
ISSN: 09559930
DOI: 10.1038/ijir.2012.39
Appears in Collections:Staff Publications

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