Demonstration of a Humoral Inhibitor of the Na+‐K+ Pump in Some Models of Experimental Hypertension
Demonstration of a Humoral Inhibitor of the Na+‐K+ Pump in Some Models of Experimental Hypertension
复制标题
Na+-K+ 泵体液抑制剂在某些实验性高血压模型中的演示
DOI：
10.1161/01.hyp.3.6_pt_2.ii-96
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发表时间：
1981
期刊：
影响因子：
8.3
通讯作者：
F. Haddy
中科院分区：
文献类型：
--
作者：
S. Huot;J. Buggy;D. Clough;F. Haddy
总结我们之前已经表明，哇巴因敏感的MRb摄取，Na+-K+泵活性的测量，在一个肾脏，一个包裹高血压的狗和一个肾脏，DOCA，盐水高血压的大鼠的血管中减少。我们在此将研究扩展到单肾、单夹和肾质量减少的大鼠-盐性高血压。我们还分析了从这些模型中的三个哇巴因敏感的uRb摄取抑制活性煮沸血浆的上清液。最后，我们研究了大鼠前腹侧第三脑室（AV 3V）损伤对血管泵和血浆上清液活动的影响。我们发现，哇巴因敏感的MRb摄取抑制在大鼠的尾动脉与一个肾，一个剪辑和减少肾质量高血压和血浆上清液从这些大鼠和狗与一个肾，一个包裹高血压抑制MRb摄取时，适用于正常大鼠的尾动脉。我们还发现，在体积扩张状态下，AV 3V病变大鼠的血管哇巴因敏感性MRb摄取高于假病变大鼠，并且有证据表明血浆抑制活性降低。这些研究结果表明，血管Na+-K+泵活性降低是常见的几种模型的实验性高血压，这种缺陷的结果从一个热稳定的哇巴因样剂在血浆中，起源于或影响的AV 3V区域的大脑。（高血压3（增刊II）：II-96-II-101，1981）
SUMMARY We have previously shown that ouabaln-sensitive MRb uptake, a measure of Na+-K+ pump activity, is decreased in the blood vessels of dogs with one-kidney, one wrapped hypertension and rats with onekidney, DOCA, saline hypertension. We here extend the study to rats with one-kidney, one clip and reduced renal mass-saline hypertension. We also assayed supernates of boiled plasma from three of these models for ouabain-sensitive uRb uptake suppressing activity. Finally, we examined the influence of the anteroventral third ventricle (AV3V) lesion in the rat on vascular pump and plasma supernate activities. We found that ouabain-sensitive MRb uptake is suppressed in the tail arteries of rats with one-kidney, one clip and reduced renal mass hypertension and that plasma supernates from these rats and from dogs with one-kidney, one wrapped hypertension suppress MRb uptake when applied to tail arteries from normal rats. We also found that, in the volume-expanded state, rats with AV3V lesions had higher vascular ouabain-sensitive MRb uptake than rats with sham lesions and evidence for decreased inhibitory activity of the plasma. These findings suggest that reduced vascular Na+-K+ pump activity is common to several models of experimental hypertension and that this defect results from a heat-stable ouabain-like agent in plasma that originates in or is influenced by the AV3V area of the brain. (Hypertension 3 (suppl II): II-96-II-101, 1981)