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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Involvement of the Na+-independent Cl–/HCO3– exchange (AE) isoform in the compensation of myocardial Na+/H+ isoform 1 hyperactivity in spontaneously hypertensive rats.
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Involvement of the Na+-independent Cl–/HCO3– exchange (AE) isoform in the compensation of myocardial Na+/H+ isoform 1 hyperactivity in spontaneously hypertensive rats.

机译：自发性高血压大鼠中独立于Na +的Cl– / HCO3–交换（AE）同种型参与心肌Na + / H +同种型1过度活跃的补偿。

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摘要

Enhanced activity of Na+/H+ isoform 1 (NHE-1) and the Na+-independent Cl–/HCO3– exchange (AE) is a feature of the hypertrophied myocardium in spontaneously hypertensive rats (SHR). The present study explored the possibility that sustained intracellular acidosis due to increased myocardial acid loading through AE causes NHE-1 enhancement. To this aim, SHR were treated for 2 weeks with a rabbit polyclonal antibody against an AE3 isoform that was recently developed and proven to have inhibitory effects on myocardial AE activity. We then compared the AE activity in the left ventricle papillary muscles isolated from untreated SHR with antiAE3-treated SHR; AE activity was measured in terms of the rate of intracellular pH recovery after an intracellular alkali load was introduced. AE activity was diminished by ~ 70% in SHR treated with the antiAE3 antibody, suggesting that the AE3 isoform is a major carrier of acid-equivalent influx in the hypertrophied myocardium. However, the antibody treatment failed to normalize NHE-1 activity that remained elevated in the myocardium of normotensive rats. The data therefore rule out the possibility that NHE-1 hyperactivity in hypertensive myocardium was due to sustained intracellular acidosis induced by increased AE activity that characterizes SHR myocardial tissue.
机译：Na + / H +同工型1（NHE-1）和不依赖Na +的Cl– / HCO3–交换（AE）的活性增强是自发性高血压大鼠（SHR）心肌肥大的特征。本研究探讨了由于通过AE增加心肌酸负荷而引起的持续细胞内酸中毒引起NHE-1增强的可能性。为了这个目的，用抗AE3亚型的兔多克隆抗体将SHR治疗了2周，该抗体最近被开发出来并被证明对心肌AE活性具有抑制作用。然后，我们将未经治疗的SHR与经抗AE3治疗的SHR分离的左心室乳头肌的AE活性进行了比较;根据引入细胞内碱负荷后细胞内pH恢复速率来测量AE活性。在用抗AE3抗体处理的SHR中，AE活性降低了约70％，这表明AE3亚型是肥大心肌中酸当量流入的主要载体。但是，抗体治疗未能使正常血压大鼠心肌中仍保持升高的NHE-1活性正常化。因此，该数据排除了高血压心肌中NHE-1过度活跃的可能是由于以SHR心肌组织为特征的AE活性增加引起的持续的细胞内酸中毒。

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