Direct Effect of Carbon Monoxide on Relaxation Induced by Electrical Field Stimulation in Rat Corpus Cavernosum.
10.4111/kju.2010.51.8.572
- Author:
Dae Woong KIM
1
;
Chen ZHAO
;
Myung Ki KIM
;
Jong Kwan PARK
Author Information
1. Department of Urology, Chonbuk National University Medical School, Jeonju, Korea. rain@chonbuk.ac.kr
- Publication Type:Original Article
- Keywords:
Carbon monoxide;
Cyclic GMP;
Electric stimulation;
Muscle relaxation;
Penile erection
- MeSH:
Animals;
Atropine;
Carbon;
Carbon Monoxide;
Contracts;
Cyclic GMP;
Electric Stimulation;
Heme;
Heme Oxygenase (Decyclizing);
Isotonic Solutions;
Male;
Muscle Relaxation;
Muscle, Smooth;
Nerve Fibers;
Nitric Oxide;
Nitric Oxide Synthase;
Penile Erection;
Phenylephrine;
Rats;
Receptors, Muscarinic;
Relaxation;
Synaptic Transmission;
Transducers;
Zinc
- From:Korean Journal of Urology
2010;51(8):572-578
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Carbon monoxide (CO) may mediate smooth muscle relaxation in the rat corpus cavernosum smooth muscle (CCSM). We hypothesized that CO plays a role in neurally derived, frequency-dependent relaxation of rat CCSM. MATERIALS AND METHODS: To study the effect of CO on CCSM relaxation induced by electrical field stimulation (EFS), a CCSM bundle was mounted on a force transducer and perfused with Hanks' balanced salt solution at 37degrees C with 95% O2 and 5% CO2. After 1 hour equilibration with -500 mg of passive tension, contraction of the CCSM bundle was elicited by 10(-5) M phenylephrine, which was continuously added with different concentrations of CO (1%, 2%, and 5%). Frequency-dependent relaxation was induced by EFS trains (0.2 ms at 0.5-32 Hz, for 10 s) repeated at 2 min intervals over 15 min in the presence of adrenergic and muscarinic receptor blocking agents (guanethidine and atropine, respectively). To study the distribution of heme oxygenase-2 (HO-2) in the rat CCSM, we performed immunohistochemical evaluation. RESULTS: CO produced a dose-dependent enhancement of EFS-induced relaxation. Pretreatment with N(G)-nitro-L-arginine (a nitric oxide synthase blocker) greatly reduced the EFS-induced relaxation in the presence of CO (-45%). Pretreatment with zinc protoporphyrin-IX (ZnPP-9, a heme oxygenase inhibitor) had no significant effect on EFS-induced relaxation in the absence or the presence of CO. We found immunoreactivity for HO-2 in CCSM and immunoreactivity for protein gene product 9.5 (PGP 9.5) in nerve fibers. CONCLUSIONS: We conclude that CO produced a dose-dependent enhancement of EFS-induced relaxation in rat CCSM bundles, but neurally derived, frequency-dependent relaxation in the rat CCSM depended mostly on nitric oxide in response to nonadrenergic noncholinergic neurotransmission. Immunoreactivity for HO-2 was found in rat CCSM but not nerve fibers.
