Vasopressin and ANG II in the control of ACTH secretion and arterial and atrial pressures.

Vasopressin and ANG II in the control of ACTH secretion and arterial and atrial pressures.
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加压素和 ANG II 控制 ACTH 分泌以及动脉和心房压力。

DOI:
10.1152/ajpregu.1989.256.2.r339
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发表时间:
1989
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Brooks,VL
Brooks,VL
中科院分区:
--
文献类型:
--
作者:
Brooks,VL

文献摘要

被引文献

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低血压会刺激促肾上腺皮质激素 (ACTH) 和加压素 (AVP) 的分泌,并增加血浆血管紧张素 II (ANG II) 的水平。由于AVP和ANG II增加ACTH分泌,因此进行本实验以评估这些肽在清醒狗中低血压引起的血浆ACTH和糖皮质激素浓度增加中的作用。这是通过确定给予加压素受体拮抗剂[1-(β-巯基-β,β-环戊亚甲基丙酸)、2-(O-甲基)酪氨酸]Arg8-加压素和ANG II (saralasin)是否会降低对四剂血管扩张剂硝普钠输注的ACTH和糖皮质激素反应来完成的。硝普钠(NP)输注产生剂量依赖性平均动脉压下降。在用AVP拮抗剂或用saralasin和加压素拮抗剂预处理的狗中,动脉压产生了更大的降低。左心房压力和右心房压力也随着 NP 输注而下降,并且在用 AVP 拮抗剂预处理的狗中发现心房压力下降幅度更大。最后,NP输注增加血浆糖皮质激素浓度和血浆ACTH浓度。在给予 AVP 拮抗剂的狗和同时给予萨拉拉辛和 AVP 拮抗剂的狗中,糖皮质激素和 ACTH 对低血压的反应均降低,但单独 AVP 阻断的效果与 AVP 和 ANG II 联合阻断的效果没有差异。这些数据表明,糖皮质激素和 ACTH 对低血压的正常反应需要 AVP,而不是 ANG II。他们还表明,AVP 对于 NP 输注期间动脉血压和心房压的正常维持是必要的。
Hypotension stimulates the secretion of adrenocorticotropin (ACTH) and vasopressin (AVP) and increases plasma levels of angiotensin II (ANG II). Because AVP and ANG II increase ACTH secretion, the present experiments were performed to evaluate the role of these peptides in the increases in plasma ACTH and glucocorticoid concentrations produced by hypotension in conscious dogs. This was accomplished by determining whether administration of receptor antagonists to vasopressin, [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]Arg8-vasopressin, and ANG II (saralasin), reduced the ACTH and glucocorticoid responses to infusion of four doses of the vasodilator nitroprusside. Nitroprusside (NP) infusion produced dose-dependent decreases in mean arterial pressure. Larger decreases in arterial pressure were produced in dogs pretreated with the AVP antagonist or with both saralasin and the vasopressin antagonist. Left and right atrial pressures also fell with NP infusion, and larger decreases in atrial pressures were found in dogs pretreated with the AVP antagonist. Finally, NP infusion increased plasma glucocorticoid concentration and plasma ACTH concentration. Both the glucocorticoid and the ACTH responses to hypotension were reduced in dogs given the AVP antagonist and in dogs given both saralasin and the AVP antagonist, but there was no difference in the effect of AVP blockade alone vs. the effect of combined AVP and ANG II blockade. These data suggest that AVP, but not ANG II, is required for normal glucocorticoid and ACTH responses to hypotension. They also suggest that AVP is necessary for normal maintenance of arterial blood pressure and atrial pressures during NP infusion.