Abstract

IntroductionCarpolobia lutea root extract (CLRE) has been reported to enhance penile erection. However, the mechanism involved is poorly understood. We investigated in vitro mechanisms of CLRE action on contractile activity of rabbit corpus cavernosum (CC). MethodsCorpus cavernosum strips from four healthy male New Zealand rabbits (2.5–3.0kg) were mounted on an organ chamber and contracted with phenylephrine (PE) (10−9 to 10−5M) and Potassium Chloride (KCl) (10–50mM) before treatment with various concentrations of CLRE (0.1–1.2mg/ml). Interactions between CLRE and a Nitric Oxide Synthase (NOS) inhibitor (N-nitro-l-arginine methyl ester – l-NAME 10−4M); guanylyl cyclase inhibitors (Oxalodiazolo 4,3-a quinoxalin-1-one – ODQ 10μM, 20μM, 30μM), and (methylene blue 10–30μM); a cyclooxygenase inhibitor (10−4M indomethacin); potassium-channel inhibitors (100μM tetraethyl ammonium TEA), (100ηM apamin) and (glibenclamide 10μM and 20μM); and a calcium-channel inhibitor (−10−4M nifedipine) were investigated. ResultsMaximal contractions of KCl and PE contracted CC strips were significantly reduced in a concentration-dependent manner (40.8±3.6% and 38.6±4.0% from 64.6±2.9% and 98.1±4.2% respectively). Relaxant effect of CLRE was significantly reduced by ODQ (38.6±4.0% to 6.4±1.3% and 38.6±4.0% to 7.2±1.2%), nifedipine (38.6±4.0% to 21.1±2.7%) and glibenclamide (40.8±3.6% to 31.5±3.3%). However l-NAME, indomethacin, methylene blue, TEA and apamin did not inhibit relaxation by CLRE. ConclusionConcentration-dependent relaxant effect of CLRE in rabbit CC involves the soluble guanylate cyclase/cyclase Guanosine Monophosphate system, and activation of ATP-dependent K+ channels.

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