Overbeck H W
Department of Medicine, University of Alabama, Birmingham 35294.
Hypertension. 1987 Nov;10(5 Pt 2):I95-100. doi: 10.1161/01.hyp.10.5_pt_2.i95.
We assessed the role of putative circulating ouabainlike factor(s) on in vivo arteriolar function in rats with very early (less than 7 days; mean, 3 days) and chronic (greater than 4 weeks) benign, one-kidney, one clip (1K1C) hypertension. Thus, we measured vascular responses in vasodilated (nitroprusside or adenosine), vascularly isolated, innervated hindlimb vascular beds of chloralose-anesthetized 1K1C rats perfused with their own blood at 1 ml/min. Complete norepinephrine dose-response curves in 8 rats with chronic and 28 with early 1K1C hypertension, compared with appropriate normotensive control rats, showed unchanged thresholds and ED50 values. Magnitude of ouabain-induced leftward shifts of the norepinephrine dose-response curve in 18 rats with chronic and 21 with early 1K1C hypertension, compared with appropriate normotensive control rats, was unchanged. Blockade of neural uptake of norepinephrine by desimipramine (10(-7) M) in 8 1K1C rats did not alter these results. These findings provide no evidence in this form and these stages of hypertension that humoral ouabainlike inhibitors of the Na+-K+ pump evoke physiologically significant inotropic effects in arterioles in vivo. It is possible, however, that induction of vascular Na+-K+-adenosine triphosphatase by circulating inhibitors modified the vascular responses to norepinephrine and ouabain in these rats.
我们评估了假定的循环类哇巴因因子在非常早期（少于7天；平均3天）和慢性（超过4周）良性单肾单夹（1K1C）高血压大鼠体内小动脉功能中的作用。因此，我们在氯醛糖麻醉的1K1C大鼠的血管舒张（硝普钠或腺苷）、血管分离、有神经支配的后肢血管床中测量了血管反应，这些血管床以1毫升/分钟的速度灌注自身血液。与适当的正常血压对照大鼠相比，8只慢性1K1C高血压大鼠和28只早期1K1C高血压大鼠的完整去甲肾上腺素剂量反应曲线显示阈值和半数有效量（ED50）值未改变。与适当的正常血压对照大鼠相比，18只慢性1K1C高血压大鼠和21只早期1K1C高血压大鼠中哇巴因诱导的去甲肾上腺素剂量反应曲线左移幅度未改变。在8只1K1C大鼠中，用去甲丙咪嗪（10^(-7) M）阻断去甲肾上腺素的神经摄取并未改变这些结果。这些发现没有提供证据表明在这种形式和高血压的这些阶段，Na+-K+泵的体液类哇巴因抑制剂在体内小动脉中引起生理上显著的变力作用。然而，循环抑制剂诱导血管Na+-K+-三磷酸腺苷酶可能改变了这些大鼠对去甲肾上腺素和哇巴因的血管反应。
