Overbeck H W, Grissette D E
Hypertension. 1982 Jan-Feb;4(1):132-9. doi: 10.1161/01.hyp.4.1.132.
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.
几个实验室报告了一些证据,表明高血压患者血管平滑肌中肌膜钠泵的活性存在异常。本实验旨在研究这些变化与肾素 - 血管紧张素 - 醛固酮系统状态及体液容量之间的关系。我们在体外评估了从患有慢性单肾单夹和双肾单夹高血压的大鼠以及适当的正常血压对照大鼠新鲜切除的钠负荷尾动脉和胸主动脉中的钠泵活性。测量了在不存在(总摄取)和存在1.0 mM哇巴因(哇巴因不敏感摄取)的情况下的86Rb摄取,并计算了哇巴因敏感摄取(纳摩尔/毫克干重/18分钟)。仅在双肾单夹大鼠中血浆肾素活性增加。在高血压大鼠中,尾动脉和主动脉中哇巴因敏感和总86Rb摄取均显著增加(高达+60%)。两种形式的戈德布拉特高血压以及在处死前2至3天饮用0.9%盐水的单肾单夹高血压大鼠中,动脉组织摄取增加的幅度相似。给正常血压对照大鼠的主动脉进一步加载钠并不会增加其摄取。本研究结果没有提供钠泵活性降低的证据,反而表明在体外研究的肌膜或动脉平滑肌中泵的活性增加。这些泵活性的增加似乎与肾素 - 血管紧张素 - 醛固酮系统活性的改变、体液容量的变化或细胞内钠浓度的增加无关。可能涉及肌膜泵分子数量或浓度的增加或其周转率的增加。然而,尾动脉和主动脉的体外86Rb摄取可能无法反映体内阻力血管中钠泵活性的状态。