Senbel Amira M, Abd Elmoneim Heba M, Sharabi Fouad M, Mohy El-Din Mahmoud M
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria UniversityAlexandria, Egypt.
Front Pharmacol. 2017 May 26;8:297. doi: 10.3389/fphar.2017.00297. eCollection 2017.
Potassium channels (KCh) in corpus cavernosum play an important role in the regulation of erection. Nitric oxide (NO) acts through opening of KCh leading to hyperpolarization and relaxation. This study aims to update knowledge about the role of voltage-gated KCh (K) channels in erectile machinery and investigate their role in the control of NO action &/or synthesis in the corpus cavernosum. Tension studies using isolated rabbit corpus cavernosum (CC) strips and rat anococcygeus muscle were conducted. Results are expressed as mean ± SEM. Electric field stimulation (EFS, 2-16 Hz) evoked frequency-dependent relaxations of the PE (phenylephrine)-precontracted CC strips. At 2 Hz, EFS-induced relaxation amounted to 73.17 ± 2.55% in presence 4-AP (10 M) compared to 41.98 ± 1.45% as control. None of the other selective KCh blockers tested inhibited EFS-induced relaxation. 4-AP (10M) significantly attenuated ACh-induced relaxation of rabbit CC where dose-response curve was clearly shifted upward, and attenuated SNP- induced relaxation, for example, to 49.28 ± 4.52% compared to 65.53 ± 3.01% as control at 10 M SNP. The potentiatory effect of 4-AP on EFS was abolished or reversed in presence of N -nitro-L-arginine (L-NNA, non-selective nitric oxide synthase inhibitor, 10M, and 2 × 10M). Same results were observed in rat anococcygeus muscle which is a part of the erectile machinery in rats. This study provides evidence for the presence of prejunctional voltage-gated KCh in CC, the blockade of which may increase the neuronal synthesis of NO.
海绵体中的钾通道（KCh）在勃起调节中起重要作用。一氧化氮（NO）通过打开KCh起作用，导致超极化和松弛。本研究旨在更新关于电压门控KCh（K）通道在勃起机制中的作用的知识，并研究它们在控制海绵体中NO作用和/或合成中的作用。使用分离的兔海绵体（CC）条和大鼠肛门尾骨肌进行张力研究。结果以平均值±标准误表示。电场刺激（EFS，2 - 16 Hz）引起苯肾上腺素（PE）预收缩的CC条的频率依赖性松弛。在2 Hz时，与作为对照的41.98±1.45%相比，在存在4 - AP（10μM）的情况下，EFS诱导的松弛达到73.17±2.55%。测试的其他选择性KCh阻滞剂均未抑制EFS诱导的松弛。4 - AP（10μM）显著减弱了乙酰胆碱（ACh）诱导的兔CC松弛，其中剂量反应曲线明显向上移动，并减弱了硝普钠（SNP）诱导的松弛，例如，在10μM SNP时，与作为对照的65.53±3.01%相比，减弱至49.28±4.52%。在存在N - 硝基 - L - 精氨酸（L - NNA，非选择性一氧化氮合酶抑制剂，10μM和2×10μM）的情况下，4 - AP对EFS的增强作用被消除或逆转。在大鼠肛门尾骨肌（大鼠勃起机制的一部分）中观察到相同的结果。本研究为CC中存在节前电压门控KCh提供了证据，阻断该通道可能会增加NO的神经元合成。
