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首页> 外文期刊>Endocrinology >A Balance Theory of Peripheral Corticotropin-Releasing Factor Receptor Type 1 and Type 2 Signaling to Induce Colonic Contractions and Visceral Hyperalgesia in Rats
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A Balance Theory of Peripheral Corticotropin-Releasing Factor Receptor Type 1 and Type 2 Signaling to Induce Colonic Contractions and Visceral Hyperalgesia in Rats

机译：外周血促肾上腺皮质激素释放因子受体1型和2型信号传导诱导大鼠结肠收缩和内脏痛觉过敏的平衡理论

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Several recent studies suggest that peripheral corticotropin-releasing factor (CRF) receptor type 1 (CRF1) and CRF2 have a counter regulatory action on gastrointestinal functions. We hypothesized that the activity balance of each CRF subtype signaling may determine the changes in colonic motility and visceral sensation. Colonic contractions were assessed by the perfused manometry, and contractions of colonic muscle strips were measured in vitro in rats. Visceromotor response was determined by measuring contractions of abdominal muscle in response to colorectal distensions (CRDs) (60 mm Hg for 10 min twice with a 30-min rest). All drugs were administered through ip route in in vivo studies. CRF increased colonic contractions. Pretreatment with astressin, a nonselective CRF antagonist, blocked the CRF-induced response, but astressin(2)-B, a selective CRF2 antagonist, enhanced the response by CRF. Cortagine, a selective CRF1 agonist, increased colonic contractions. In in vitro study, CRF increased contractions of muscle strips. Urocortin 2, a selective CRF2 agonist, itself did not alter the contractions but blocked this increased response by CRF. Visceromotor response to the second CRD was significantly higher than that of the first. Astressin blocked this CRD-induced sensitization, but astressin(2)-B or CRF did not affect it. Meanwhile, astressin(2)- B together with CRF significantly enhanced the sensitization. Urocortin 2 blocked, but cortagine significantly enhanced, the sensitization. These results indicated that peripheral CRF1 signaling enhanced colonic contractility and induced visceral sensitization, and these responses were modulated by peripheral CRF2 signaling. The activity balance of each subtype signaling may determine the colonic functions in response to stress.
机译：最近的几项研究表明，外周血促肾上腺皮质激素释放因子（CRF）受体1型（CRF1）和CRF2对胃肠功能具有反调节作用。我们假设每种CRF亚型信号传导的活动平衡可能决定结肠运动和内脏感觉的变化。通过灌注测压法评估结肠收缩，并在大鼠中体外测量结肠肌条的收缩。通过测量响应结直肠扩张（CRD）（60毫米汞柱持续10分钟两次，休息30分钟）的腹肌收缩来确定内运动反应。在体内研究中，所有药物均通过ip途径给药。 CRF增加结肠收缩。用非选择性CRF拮抗剂astressin预处理可以阻断CRF诱导的反应，但是选择性CRF2拮抗剂astressin（2）-B可以增强CRF的反应。选择性CRF1激动剂Cortagine可增加结肠收缩。在体外研究中，CRF增加了肌肉条的收缩。选择性CRF2激动剂Urocortin 2本身并未改变收缩，但阻止了CRF引起的这种增加的反应。对第二个CRD的内脏动力反应明显高于第一个。 Astressin阻止了这种CRD诱导的致敏作用，但astressin（2）-B或CRF对此没有影响。同时，astressin（2）-B与CRF一起显着增强了敏化作用。 Urocortin 2受阻，但可卡汀明显增强，致敏性。这些结果表明外周CRF1信号增强结肠收缩力和诱导内脏致敏，并且这些应答被外周CRF2信号调节。每个亚型信号传导的活性平衡可以确定结肠功能以应对压力。

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