Effect of ouabain on arteriolar responses to norepinephrine in chronic, benign, volume-expanded hypertension.
Effect of ouabain on arteriolar responses to norepinephrine in chronic, benign, volume-expanded hypertension.
复制标题
哇巴因对慢性良性扩张性高血压的小动脉对去甲肾上腺素反应的影响。
DOI：
10.1161/01.hyp.6.2_pt_2.i82
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Overbeck,HW
中科院分区：
文献类型：
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作者：
Overbeck,HW
我们已经报道了从体积扩大的Dahl盐敏感（S）大鼠和慢性（4至6周）良性（血清肌酐低于1.4 mg%）单肾一夹（1 K1 C）高血压大鼠新鲜切除的导管动脉中哇巴因敏感的Rb+摄取增加。为了评估后一种模型中的体内小动脉功能，以及假定的循环哇巴因样因子的作用，我们用氯醛糖麻醉的、饮水或盐水的1 K1 C高血压大鼠自身血液以1 ml/min灌注最大血管舒张（硝普钠，0.015 mg/ml肢体血液）、血管分离、神经支配的后肢血管床，并测量肢体对i.a.去甲肾上腺素0.004至128微克，在哇巴因局部输注之前和期间（肢体血液中达到2.5 × 10（-5）M）。8只1 K1 C高血压大鼠的完整剂量-反应曲线比5只单侧肾切除（1 K）正常血压对照大鼠的更陡和更高。然而，阈值和ED 50不变。因此，高血压大鼠的曲线变化仅代表结构性血管变化。哇巴因在另外18只1 K1 C高血压大鼠和13只1 K正常血压对照大鼠中引起剂量-反应曲线的显著偏移。在高血压大鼠与对照组相比，有增加的趋势，而不是减少，在哇巴因诱导的曲线移动。在14只慢性2K 1C高血压大鼠中，这些变化与1 K1 C高血压大鼠没有差异。总之，这些在慢性、可能是容量扩张、低肾素高血压且不伴有肾功能不全的研究未提供循环哇巴因样泵抑制剂的生理学显著性变力作用的证据。
We have reported increases in ouabain-sensitive Rb+ uptake by freshly excised conduit arteries from volume-expanded Dahl salt-sensitive (S) rats and also from rats with chronic (4 to 6 weeks), benign (serum creatinine less than 1.4 mg%) one-kidney, one clip ( 1K1C ) hypertension on high NaCl intake. To assess in vivo arteriolar function in this latter model, and a role for putative circulating ouabain-like factors, we perfused the maximally vasodilated (nitroprusside, 0.015 mg/ml limb blood), vascularly isolated, innervated hindlimb vascular beds of chloralose-anesthetized, water- or saline-drinking 1K1C hypertensive rats with their own blood at 1 ml/min, and measured limb responses to i.a. norepinephrine 0.004 to 128 micrograms, before and during local infusion of ouabain (achieving 2.5 X 10(-5) M in limb blood). Complete dose-response curves in eight 1K1C hypertensive rats were steeper and higher than those in five uninephrectomized (1K) normotensive control rats. However, threshold and ED50 were unchanged. Thus, alterations in the curve in the hypertensive rats represented only structural vascular changes. Ouabain evoked a leftward shift of the dose-response curve in an additional 18 1K1C hypertensive rats and 13 1K normotensive controls. In the hypertensive rats as compared to the controls, there were trends for increases, rather than decreases, in the ouabain-induced shift of the curve. Shifts in 14 rats with chronic 2K1C hypertension did not differ from those in the 1K1C hypertensive rats. Together, these studies in chronic, presumably volume-expanded, low-renin hypertension unaccompanied by renal insufficiency provide no evidence for physiologically significant inotropic effects of circulating ouabain-like pump inhibitor.