Abstract
Aims of study. The aim of the present study was to investigate whether an ethanol extract of Scutellaria baicalensis (ESB) relaxes penile corpus cavernosum muscle in organ bath experiments. Materials and methods. Changes in tension of cavernous smooth muscle strips were determined by penile strip chamber model and in penile perfusion model. Isolated endothelium-intact rabbit corpus cavernosum was precontracted with phenylephrine (PE) and then treated with ESB. Results. ESB relaxed penile smooth muscle in a dose-dependent manner, and this was inhibited by pre-treatment with NG-nitro-l-arginine methyl ester (l-NAME), a nitric oxide (NO) synthase inhibitor, and 1H-[1, 2, 4]-oxadiazolo-[4,3-α]-quinoxalin-1-one (ODQ), a soluble guanylyl cyclase (sGC) inhibitor. ESB-induced relaxation was significantly attenuated by pretreatment with tetraethylammonium (TEA), a nonselective K+ channel blocker, and charybdotoxin, a selective Ca2+-dependent K+ channel inhibitor. ESB increased the cGMP levels of rabbit corpus cavernosum in a concentration-dependent manner without changes in cAMP levels. In a perfusion model of penile tissue, ESB also relaxed penile corpus cavernosum smooth muscle in a dose-dependent manner. Conclusion. Taken together, these results suggest that ESB relaxed rabbit cavernous smooth muscle via the NO/cGMP system and Ca2+-sensitive K+ channels in the corpus cavernosum.
Highlights
Penile erection is a hemodynamic process induced by both increased arterial inflow and restricted venous outflow and is coordinated with smooth muscle relaxation within the corpus cavernosum under neural control [1, 2]
Charybdotoxin, but not by 4-AP or glibenclamide (Figures 4(b), 4(c), and 4(d)). These findings suggest that extract of Scutellaria baicalensis (ESB) elicits cavernous smooth muscle relaxation via K+ channels, the KCa channels
The present study shows that ESB elicits the relaxation of PE-precontracted cavernous smooth muscle strips in penile corpus cavernosum smooth muscle with
Summary
Penile erection is a hemodynamic process induced by both increased arterial inflow and restricted venous outflow and is coordinated with smooth muscle relaxation within the corpus cavernosum under neural control [1, 2]. Penile tumescence and detumescence are regulated by a complex neurophysiological process involving the relaxation and contraction, respectively, of the corpus cavernosum. Erection occurs when the penile arteries and corpus cavernosal smooth muscle are relaxed by nitric oxide (NO) released from nerve endings and endothelial cells [3, 4]. CGMP is predominantly metabolized by phosphodiesterase type 5 (PDE 5). This enzyme is the most prominent target of the NO/cGMP signalling cascade identified to date for pharmacological intervention in erectile dysfunction. The NO/cGMP pathway plays a key role in penile erection
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