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    Changes in cholinergic and nitrergic systems of defunctionalized colons after colostomy in rabbits
    (Academic Press Inc Elsevier Science, 2017) Moralioglu, Serdar; Vural, Ismail Mert; Ozen, Ibrahim Onur; Ozturk, Gokce; Sarıoğlu, Yusuf; Basaklar, Abdullah Can
    Background: This study was designed to assess smooth muscle function and motility in defunctionalized colonic segments and subsequent changes in pathways responsible for gastrointestinal motility. Methods: Two-month-old New Zealand rabbits were randomly allocated into control and study groups. Sigmoid colostomies were performed in the study group. After a 2-month waiting period, colonic segments were harvested in both groups. For the in vitro experiment, the isolated circular muscle strips which were prepared from the harvested distal colon were used. First, contraction responses were detected using KCl and carbachol; relaxation responses were detected using papaverine, sodium nitroprusside, sildenafil, and L-arginine. The neurologic responses of muscle strips to electrical field stimulation (EFS) were evaluated in an environment with guanethidine and indomethacin. EFS studies were then repeated with atropine, Nu-nitro-L-arginine methyl ester, atropine, and Nu-nitro-Larginine methyl estereadded environments. Results: Although macroscopic atrophy had developed in the distal colonic segment of the colostomy, the contraction and relaxation capacity of the smooth muscle did not change. EFS-induced nitrergic-peptidergic, cholinergic-peptidergic, and noncholinergic nonnitrergic responses significantly decreased at all frequencies (0.5-32 Hz) in the study group compared with those in the control group (P < 0.05). Conclusions: Although the contraction capacity of the smooth muscle was not affected, the motility of the distal colon deteriorated owing to the defective secretion of presynaptic neurotransmitters such as acetylcholine, nitric oxide, and neuropeptides. (C) 2016 Elsevier Inc. All rights reserved.
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    Effects of cannabinoid and vanilloid receptor antagonists on nicotine induced relaxation response enhancement in rabbit corpus cavernosum
    (2022) Vural, Ismail Mert; Ozturk Fincan, Gokce Sevi; Koc, Derya Sebile; Okcay, Yagmur; Askin, Celil Ilker; Kibar, Ayse Kubra; Ilhan, Sevil Ozger; Sarıoğlu, Yusuf
    Objectives: Endocannabinoids and nicotine regulate the neurotransmitter release in different central and peripheral synapses. Various studies in the literature demonstrate the interaction between endocannabinoid and nicotinic systems, especially in the central nervous system. The interaction between nicotinic and endocannabinoid systems was investigated in this study. We aimed to show the effects of cannabinoid and vanilloid receptor antagonists on nicotine-induced relaxation response increases in rabbit corpus cavernosum. Materials and methods: From a total of seven male albino rabbits, three or four equal strips were cut from each corpus cavernosum and inserted in isolated organ baths. Tissues were contracted with phenylephrine (3×10-5 M). After contraction reached a plateau, strips were stimulated with EFS, and with the stabilization of EFS relaxation responses, 10-4 M of nicotine was administered to tissues. After that, in order to investigate the effects of AM251 (CB1 antagonist), AM630 (CB2 inverse agonist) or capsazepine (a vanilloid receptor antagonist) were given to different tissues, after the resting period. Results: Nicotine (10-4 M) increased the EFS-induced relaxation responses (14.60%±2.94%, P<0.05). AM630 decreased the enhancement of nicotine-induced EFS relaxation responses (nicotine 10-4 M enhancement: 17.16%±3.19%; nicotine 10-4 M enhancement in the presence of AM630 10-6 M: 4.44%±3.43% P<0.05; n=6), whereas effects of AM251 and capsazepine were not significant. Conclusion: In the present study, nicotine increased the amplitudes of EFS-induced relaxation responses probably via nicotinic acetylcholine receptors located on the nitrergic nerves of the corpus cavernosum. We showed the role of cannabinoid-like endo-ligands in nicotine-induced enhancement via CB2 receptors but not CB1 and VR1 receptors.