Sodium pump activity in arteries of Dahl salt-sensitive rats.
Sodium pump activity in arteries of Dahl salt-sensitive rats.
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达尔盐敏感大鼠动脉中的钠泵活性。
DOI：
10.1161/01.hyp.3.3.306
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Rapp,JP
中科院分区：
文献类型：
--
作者：
Overbeck,HW;Ku,DD;Rapp,JP
血管平滑肌的产电钠泵活性降低已在几种形式的实验性高血压中报道，并可能在基本疾病机制中发挥重要作用。已经提出，这种泵抑制可以表征高血压的体积膨胀形式。目前的调查验证了后一种假设。钠泵活性进行了评估，在体外钠负载尾动脉和胸主动脉新鲜切除Dahl盐敏感性（S）和耐盐性（R）大鼠低（0.4%）或高（8%）NaCl饮食5至7周。测量了在不存在（总摄取）和存在（哇巴因不敏感摄取）1.0 mM哇巴因的情况下的铷（86 Rb）摄取，并计算了哇巴因敏感摄取（nmole/mg干重/10 min）。在S大鼠中，盐喂养伴随着动脉压升高，心脏肥大，总血容量增加20%至30%，哇巴因敏感，哇巴因不敏感和主动脉总摄取量增加，但尾动脉摄取量无显著变化。然而，哇巴因敏感的摄取在所有S大鼠的尾动脉超过在R大鼠。没有证据表明血管钠泵活性降低伴随高血压在任何动脉。因此，本研究的结果没有提供证据支持血管平滑肌中泵抑制是高血压体积扩张形式特征的假设。在S大鼠中观察到的血管泵活性增加不太可能反映细胞内钠浓度高于对照大鼠。相反，可能涉及泵分子数量或其周转率的增加。
Decreased activity of the electrogenic sodium pump of vascular smooth muscle has been reported in several forms of experimental hypertension and may play an important role in basic disease mechanisms. It has been proposed that such pump suppression may characterize volume-expanded forms of hypertension. The present investigation tested this latter hypothesis. Sodium pump activity was assessed in vitro in sodium-loaded tail artery and thoracic aorta freshly excised from Dahl salt-sensitive (S) and salt-resistant (R) rats on low (0.4%) or high (8%) NaCl diets for 5 to 7 weeks. Rubidium (86Rb) uptake in the absence (total uptake) and presence (ouabain-insensitive uptake) of 1.0mM ouabain was measured and ouabain-sensitive uptake (nmole/mg dry weight/10 min) was calculated. In S rats, salt feeding was accompanied by elevation of arterial pressure, cardiac hypertrophy, increases of 20% to 30% in total blood volume, and increases in the ouabain-sensitive, ouabain-insensitive, and total uptakes in the aorta, but no significant change in uptakes in the tail artery. However, ouabain-sensitive uptake in the tail artery of all S rats exceeded than in R rats. There was no evidence of a decrease in vascular sodium pump activity accompanying hypertension in either artery. Therefore, the results of this study provide no evidence in support of the hypothesis that pump suppression in vascular smooth muscle characterizes volume-expanded forms of hypertension. It is unlikely that the observed increases in vascular pump activity in S rats reflected intracellular sodium concentrations higher than those in the control rats. Rather, increases in the numbers of pump molecules or in their turnover rate are probably involved.