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肥胖抑制素抑制抗利尿激素分泌:对体液平衡控制中生理作用的证据。

Obestatin inhibits vasopressin secretion: evidence for a physiological action in the control of fluid homeostasis.

作者信息

Samson Willis K, Yosten Gina L C, Chang Jaw-Kang, Ferguson Alastair V, White Meghan M

机构信息

Department of Pharmacological and Physiological Science, Saint Louis University, 1402 South Grand Boulevard, St Louis, Missouri 63104, USA.

出版信息

J Endocrinol. 2008 Mar;196(3):559-64. doi: 10.1677/JOE-07-0364.

DOI:10.1677/JOE-07-0364
PMID:18310451
Abstract

Obestatin, a product of post-translational processing of the ghrelin prohormone, has been reported to act in the brain to inhibit thirst. We extended our initial studies on water drinking by examining the effects of obestatin on hypovolemia-induced water and saline drinking and vasopressin release in male rats. Intracerebroventricular administration of obestatin significantly inhibited water, but not saline (0.3 M NaCl) drinking in response to a hypovolemic challenge. Obestatin also inhibited, in a dose-related fashion, dehydration-induced vasopressin secretion without affecting plasma oxytocin levels. Vasopressin release induced by central angiotensin II administration was attenuated significantly by prior administration of obestatin. Finally, central administration of an antiserum specific to obestatin resulted in an exaggerated basal vasopressin release and an increased vasopressin response to overnight water deprivation. Antiserum treatment also resulted in significantly increased ad libitum water drinking and drinking in response to dehydration. We conclude that this product of post-translational processing of the ghrelin prohormone may be an important contributor to the physiologic regulation of fluid and electrolyte homeostasis.

摘要

胃饥饿素原经翻译后加工产生的胃抑素,据报道可在大脑中发挥作用以抑制口渴。我们通过研究胃抑素对雄性大鼠低血容量诱导的饮水和盐水摄入以及抗利尿激素释放的影响,扩展了我们最初关于饮水的研究。脑室内注射胃抑素可显著抑制低血容量刺激引起的饮水,但不影响盐水(0.3M NaCl)摄入。胃抑素还以剂量相关的方式抑制脱水诱导的抗利尿激素分泌,而不影响血浆催产素水平。预先注射胃抑素可显著减弱中枢给予血管紧张素II诱导的抗利尿激素释放。最后,中枢注射胃抑素特异性抗血清导致基础抗利尿激素释放增加以及对过夜禁水的抗利尿激素反应增强。抗血清处理还导致随意饮水和脱水后饮水显著增加。我们得出结论,胃饥饿素原经翻译后加工产生的该产物可能是体液和电解质稳态生理调节的重要贡献者。

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