Carneiro Fernando S, Giachini Fernanda R C, Lima Victor V, Carneiro Zidonia N, Nunes Kênia P, Ergul Adviye, Leite Romulo, Tostes Rita C, Webb R Clinton
Medical College of Georgia, Department of Physiology, 1120 Fifteenth Street, CA-3141, Augusta, GA 30912-3000, USA.
Can J Physiol Pharmacol. 2008 Jun;86(6):320-8. doi: 10.1139/Y08-031.
The penis is kept in the flaccid state mainly via a tonic activity of norepinephrine and endothelins (ETs). ET-1 is important in salt-sensitive forms of hypertension. We hypothesized that cavernosal responses to ET-1 are enhanced in deoxycorticosterone acetate (DOCA)-salt mice and that blockade of ETA receptors prevents abnormal responses of the corpus cavernosum in DOCA-salt hypertension. Male C57BL/6 mice were unilaterally nephrectomized and treated for 5 weeks with both DOCA and water containing 1% NaCl and 0.2% KCl. Control mice were uninephrectomized and received tap water with no added salt. Animals received either the ETA antagonist atrasentan (5 mg x day(-1) x kg(-1) body weight) or vehicle. DOCA-salt mice displayed increased systolic blood pressure (SBP), and treatment with atrasentan decreased SBP in DOCA-salt mice. Contractile responses in cavernosal strips from DOCA-salt mice were enhanced by ET-1, phenylephrine, and electrical field stimulation (EFS) of adrenergic nerves, whereas relaxations were not altered by IRL-1620 (an ETB agonist), acetylcholine, sodium nitroprusside, and EFS of nonadrenergic noncholinergic nerves. PD59089 (an ERK1/2 inhibitor), but not Y-27632 (a Rho-kinase inhibitor), abolished enhanced contractions to ET-1 in cavernosum from DOCA-salt mice. Treatment of DOCA-salt mice with atrasentan did not normalize cavernosal responses. In summary, DOCA-salt treatment in mice enhances cavernosal reactivity to contractile, but not to relaxant, stimuli, via ET-1/ETA receptor-independent mechanisms.
阴茎主要通过去甲肾上腺素和内皮素(ETs)的紧张性活动维持在疲软状态。ET-1在盐敏感性高血压类型中起重要作用。我们假设,在醋酸脱氧皮质酮(DOCA)-盐负荷小鼠中,海绵体对ET-1的反应增强,并且ETA受体阻断可预防DOCA-盐负荷高血压中海绵体的异常反应。雄性C57BL/6小鼠单侧肾切除,并用DOCA和含1% NaCl和0.2% KCl的水治疗5周。对照小鼠单侧肾切除并给予无添加盐的自来水。动物接受ETA拮抗剂阿曲生坦(5 mg×天⁻¹×kg⁻¹体重)或赋形剂。DOCA-盐负荷小鼠收缩压(SBP)升高,阿曲生坦治疗可降低DOCA-盐负荷小鼠的SBP。ET-1、去氧肾上腺素和肾上腺素能神经的电场刺激(EFS)增强了DOCA-盐负荷小鼠海绵体条带的收缩反应,而IRL-1620(一种ETB激动剂)、乙酰胆碱、硝普钠和非肾上腺素能非胆碱能神经的EFS对舒张反应无影响。PD59089(一种ERK1/2抑制剂)而非Y-27632(一种Rho激酶抑制剂)消除了DOCA-盐负荷小鼠海绵体对ET-1增强的收缩反应。用阿曲生坦治疗DOCA-盐负荷小鼠并未使海绵体反应恢复正常。总之,小鼠DOCA-盐负荷治疗通过不依赖ET-1/ETA受体的机制增强了海绵体对收缩性刺激而非舒张性刺激的反应性。