Sodium pump activity in arteries of rats with Goldblatt hypertension.
Sodium pump activity in arteries of rats with Goldblatt hypertension.
复制标题
戈德布拉特高血压大鼠动脉钠泵活性。
DOI：
10.1161/01.hyp.4.1.132
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Grissette,DE
中科院分区：
文献类型：
--
作者：
Overbeck,HW;Grissette,DE
几个实验室报告的证据表明，高血压患者血管平滑肌中的肌膜钠泵活动异常。本实验旨在研究这种变化与肾素-血管紧张素-醛固酮系统状态和体液容量的关系。我们评估了慢性一肾一夹和两肾一夹高血压大鼠和正常血压对照组大鼠新鲜切除的尾动脉和胸主动脉钠泵的体外活性。测量无哇巴因(总摄取)和存在1.0 mM哇巴因(哇巴因不敏感摄取)时的86Rb摄取，并计算哇巴因敏感摄取(nmole/mg干重/18min)。两肾一夹大鼠血浆肾素活性升高。在高血压大鼠，尾动脉和主动脉对哇巴因的敏感性和86Rb摄取显著增加(高达+60%)。在两种Goldblatt高血压模型中，动脉组织摄取的增加幅度与单肾高血压大鼠相似，单肾高血压大鼠在处死前给予0.9%生理盐水2-3天。此外，正常血压对照组大鼠的主动脉钠负荷并没有增加它们的摄取。这项研究的结果并没有提供钠泵活性降低的证据，相反，这表明在体外研究的肌膜或动脉平滑肌中钠泵的活性增加。泵活性的这些增加似乎与肾素-血管紧张素-醛固酮系统的活性变化、体液容量的变化或细胞内钠浓度的增加无关。肌膜泵分子的数量或浓度的增加或其周转率的增加可能是相关的。然而，在体外，尾动脉和主动脉对86Rb的摄取可能不能反映体内阻力血管的钠泵活动状态。
Several laboratories have reported evidence suggesting abnormalities in the activity of the sarcolemmal sodium pump in vascular smooth muscle in hypertension. The present experiments were designed to investigate the relationship of such changes to the status of the renin-angiotensin-aldosterone system and body fluid volumes. We assessed sodium pump activity in vitro in sodium-loaded tail artery and thoracic aorta freshly excised from rats with chronic one-kidney, one clip, and two-kidney, one clip hypertension, and from appropriate normotensive control rats. 86Rb uptake in the absence (total uptake) and presence of 1.0 mM ouabain (ouabain-insensitive uptake) was measured, and ouabain-sensitive uptake (nmole/mg dry weight/18 min) was calculated. There were increases in plasma renin activity in the two-kidney, one clip rats only. In the hypertensive rats there were significant increases (up to +60%) in the ouabain-sensitive and total 86Rb uptakes in both tail artery and aorta. The magnitude of increases in arterial tissue uptakes in the two forms of Goldblatt hypertension, and in one-kidney, one clip hypertensive rats given 0.9% saline to drink for 2 to 3 days before sacrifice, were similar. Further sodium loading of aortas from normotensive control rats did not increase their uptake. The results of this study provide no evidence for decreases in sodium pump activity, instead indicating that there are increases in the activity of the pump in the sarcolemma or arterial smooth muscle studied in vitro. These increases in pump activity do not appear to be related to altered activity of the renin-angiotensin-aldosterone system, to changes in body fluid volumes, or to increases in intracellular concentrations of sodium. Increases in numbers or concentration of sarcolemmal pump molecules or in their turnover rate may be involved. However, in vitro 86Rb uptake by tail artery and aorta may not reflect the status of sodium pump activity in resistance vessels in vivo.