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首页> 外文会议>International Symposium on Catecholamines and Other Neurotransmitters in Stress >Vasopressin Does Not MediateHypersensitivity of the HypothalamicPituitary Adrenal Axis during Chronic Stress
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Vasopressin Does Not MediateHypersensitivity of the HypothalamicPituitary Adrenal Axis during Chronic Stress

机译：在慢性胁迫期间，VasoPressin不会介导下丘脑垂体肾上腺轴的超敏反应

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The hypothesis that vasopressin (VP) becomes the main mediator of pituitary corti-cotroph responsiveness during chronic hypothalamic pituitary adrenal (HPA) axis ac-tivation was tested by examining the effect of pharmacologic VP receptor blockade on the adrenocorticotropic hormone (ACTH) and corticosterone responses of 14-day repeatedly restrained rats. In spite of the increased vasopressinergic activity, repeat-edly restrained rats showed lower ACTH and corticosterone responses to 10 min white noise compared with handled controls. These responses were unchanged by injection of the nonpeptide-selective Vlb receptor antagonist SSR149415 i.v., 1 h before noise ap-plication. In contrast to noise stress, plasma ACTH responses to i.p. hypertonic saline injection were enhanced in the repeatedly restrained rats compared with handled con-trols, but responses were also unaffected by SSR149415 administered orally, daily 1 h before restraint. Since SSR149415 effectiveness was low, we used minipump infusion of the peptide VI receptor antagonist, dGly[Phaal,D-tyr(et), Lys, Arg]VP (V1-Ant) for 14 days, which effectively blocked ACTH responses to exogenous VP. Chronic V1-Ant infu-sion reduced plasma ACTH responses to i.p. hypertonic saline in handled controls but not in repeatedly restrained rats. These data suggest that the increased vasopressinergic activity characteristic of chronic stress plays roles other than mediating the hypersen-sitivity of the HPA axis to a novel stress.
机译：该加压素（VP）变成慢性丘脑 - 垂体 - 肾上腺（HPA）期间垂体科尔蒂-cotroph响应的主要介体轴AC-tivation通过检查对促肾上腺皮质激素（ACTH）和皮质酮反应药理VP受体阻断的效果测试的假设14天的反复抑制大鼠。尽管增加的加压素活性，重复edly内敛大鼠处理对照组相比，显示出较低的ACTH和皮质酮反应，10分钟的白噪声。这些反应是不变通过非肽选择性VIb族受体拮抗剂SSR149415静脉内注射，噪声AP-折叠之前1个小时。在对比度噪声应力，血浆ACTH响应腹膜内高渗盐水注射液在反复受约束的大鼠加强与处理CON-trols相比，但反应也不受SSR149415约束前1个小时口服给药时，每日。由于SSR149415效力是低的，我们使用的肽VI受体拮抗剂，dGly微泵输注[Phaal，d-Tyr（乙基），赖氨酸，精氨酸] VP（V1-ANT），持续14天，其有效地阻挡ACTH响应外源性VP 。慢性V1-ANT infu-锡永降低的血浆ACTH响应腹膜内高渗盐水在处理控制，但没有反复克制作用。这些数据表明，慢性应激的增加的加压素活性特性起着比介导HPA轴的hypersen-敏度的新型应力其他角色。

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