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精氨酸加压素和血管紧张素II对麻醉缺水大鼠体循环动脉压维持的相对贡献。

Relative contributions of arginine vasopressin and angiotensin II to maintenance of systemic arterial pressure in the anesthetized water-deprived rat.

作者信息

Andrews C E, Brenner B M

出版信息

Circ Res. 1981 Feb;48(2):254-8. doi: 10.1161/01.res.48.2.254.

DOI:10.1161/01.res.48.2.254
PMID:7006848
Abstract

We used a structural analogue of arginine vasopressin (AVP) and investigated the role of AVP in the maintenance of mean arterial pressure (AP) in anesthetized, water-deprived rats. The administration of [1(beta-mercapto-beta,beta-cyclopentamethylene propionic acid) 4-valine-8-D-arginine] vasopressin, d(CH2)5VDAVP, completely inhibited to 30-40 mma Hg rise in AP which normally accompanied the administration of 50 mU exogenous AVP (group 1). Thus, d(CH2)5VDAVP is a specific antagonist of the vascular effects of AVP. d(CH2)5VDAVP failed to significantly alter AP in water diuretic rats (group 3) and was without effect on urine osmolality during water diuresis or antidiuresis. However, bolus injection of d(CH2)5VDAVP into water deprived rats (group 2) prompted an abrupt fall in AP from 112 +/- 4 to 94 +/- 4 mm Hg (P less than 0.001). This fall in AP was transient, with return of AP to 110 +/- 4 mm Hg within 15 minutes. Administration of saralasin, an angiotensin II antagonist, not only prevented the compensation in AP, but also significantly magnified the maximal hypotensive response seen following d(CH2)5VDAVP (group 4). Discontinuing the saralasin allowed AP to return to baseline. Bilateral nephrectomy (group 5) also prevented the return of AP, further implicating endogenous angiotensin II as the specific mediator of the compensation in AP following d(CH2)5VDAVP administration. These studies clearly demonstrate that circulating AVP contributes to the maintenance of AP during water deprivation in the anesthetized rat. When this vascular action of AVP is blocked, angiotensin II assumes major responsibility for blood pressure regulation in the antidiuretic state.

摘要

我们使用了精氨酸加压素(AVP)的一种结构类似物,并研究了AVP在麻醉、缺水大鼠平均动脉压(AP)维持中的作用。给予[1(β-巯基-β,β-环戊亚甲基丙酸)4-缬氨酸-8-D-精氨酸]加压素,即d(CH2)5VDAVP,可完全抑制通常伴随给予50 mU外源性AVP出现的AP升高至30 - 40 mmHg(第1组)。因此,d(CH2)5VDAVP是AVP血管效应的特异性拮抗剂。d(CH2)5VDAVP未能显著改变水利尿大鼠的AP(第3组),且对水利尿或抗利尿期间的尿渗透压无影响。然而,向缺水大鼠(第2组)静脉注射d(CH2)5VDAVP促使AP从112±4 mmHg突然降至94±4 mmHg(P<0.001)。这种AP下降是短暂的,15分钟内AP恢复至110±4 mmHg。给予血管紧张素II拮抗剂沙拉新,不仅可防止AP的代偿,还能显著放大d(CH2)5VDAVP后的最大降压反应(第4组)。停用沙拉新后AP恢复至基线。双侧肾切除(第5组)也可防止AP恢复,进一步表明内源性血管紧张素II是给予d(CH2)5VDAVP后AP代偿的特异性介质。这些研究清楚地表明,循环中的AVP有助于麻醉大鼠缺水期间AP的维持。当AVP的这种血管作用被阻断时,血管紧张素II在抗利尿状态下承担血压调节的主要责任。

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