We recently demonstrated that peripheral and central administration of nesfatin-1 in fasting and satiety states generate hyperventilation activity by increasing tidal volume (TV), respiratory rate (RR), and respiratory minute ventilation (RVM). The present study aimed to investigate the mediation of central cholinergic receptors effective in respiratory control in the hyperventilation activity of nesfatin-1. Besides this, we intended to determine possible changes in blood gases due to hyperventilation activity caused by nesfatin-1 and investigate the mediation of central cholinergic receptors in these changes.

Intracerebroventricular (ICV) administration of nesfatin-1 revealed a hyperventilation response with an increase in TV, RR, RMV, and pO₂ and a decrease in pCO₂ in saturated Sprague Dawley rats. ICV pretreatment with the muscarinic receptor antagonist atropine partially blocked the RR, RMV, pO₂, and pCO₂ responses produced by nesfatin-1 while completely blocking the TV response. However, central pretreatment with nicotinic receptor antagonist mecamylamine blocked the respiratory and blood gas responses induced by nesfatin-1.

The study's conclusion demonstrated that nesfatin-1 had active hyperventilation effects resulting in an increase in pO₂ and a decrease in pCO₂. The critical finding of the study was that activation of central cholinergic receptors was involved in nesfatin-1-evoked hyperventilation and blood gas responses.

我们最近证明，在空腹和饱腹状态下外周和中枢给药 nesfatin-1 通过增加潮气量 (TV)、呼吸频率 (RR) 和呼吸分钟通气量 (RVM) 产生过度换气活动。本研究旨在探讨中枢胆碱能受体在 nesfatin-1 过度换气活动中对呼吸控制有效的介导作用。除此之外，我们还打算确定由 nesfatin-1 引起的过度换气活动可能导致的血气变化，并研究中枢胆碱能受体在这些变化中的介导作用。

nesfatin-1 的脑室内 (ICV) 给药显示过度通气反应，饱和 Sprague Dawley 大鼠的 TV、RR、RMV 和 pO ₂增加， pCO _2降低。用毒蕈碱受体拮抗剂阿托品预处理ICV部分阻断由nesfatin-1产生的RR、RMV、pO ₂和pCO ₂反应，同时完全阻断TV反应。然而，用烟碱样受体拮抗剂美加明进行中枢预处理阻断了由 nesfatin-1 诱导的呼吸和血气反应。

该研究的结论表明，nesfatin-1 具有积极的过度换气作用，导致 pO ₂增加和 pCO ₂降低。该研究的关键发现是中枢胆碱能受体的激活与 nesfatin-1 诱发的过度换气和血气反应有关。