Jelicks L A, Gupta R K
Department of Physiology and Biophysics, Albert Einstein College of Medicine of Yeshiva University, Bronx, New York 10461.
Am J Hypertens. 1994 May;7(5):429-35. doi: 10.1093/ajh/7.5.429.
We have used 23Na nuclear magnetic resonance spectroscopy to examine the relationship between intracellular sodium and cardiac muscle alterations in genetic hypertension. In the spontaneously hypertensive rat (SHR) compared with the normotensive Wistar-Kyoto rat (WKY) (aged 15 to 19 weeks), mean systolic blood pressures (measured using the tail-cuff method) were significantly (P < .05) different (WKY: 118 +/- 8 mm Hg, n = 5; SHR: 185 +/- 9 mm Hg, n = 5). Heart weights were also increased significantly (P < .05) in SHR (grams dry heart to kilograms body weight ratio was 0.73 +/- 0.04, n = 5, for SHR and 0.55 +/- 0.02, n = 5, for WKY). Intracellular sodium levels, measured using shift-reagent-aided and triple quantum filtered (TQF) nuclear magnetic resonance techniques, were significantly increased (P < .05) in the isolated Langendorff perfused hypertensive rat hearts (17.3 +/- 3.6 mmol/L, n = 5) compared with normotensive rat hearts (8.4 +/- 2.3 mmol/L, n = 5). These data demonstrate increased sodium in cardiac muscle in essential hypertension. We also investigated the effect of pacing on cardiac TQF 23Na nuclear magnetic resonance and found an increase in TQF Na+ content in both WKY and SHR hearts on stepped up pacing. These results support the existence of sodium pump lag in the rat heart perfused at physiologic Ca2+ concentration and suggest that the hypertensive rat heart has adapted to compensate for increased basal intracellular Na+ and maintain a normal response to increased heart rate. Our data appear to suggest an ionic contribution to the cardiac hypertrophy of genetic hypertension in the rat.
我们运用23Na核磁共振波谱技术来研究遗传性高血压中细胞内钠与心肌改变之间的关系。与正常血压的Wistar-Kyoto大鼠（WKY）（15至19周龄）相比，自发性高血压大鼠（SHR）的平均收缩压（采用尾套法测量）存在显著差异（P < 0.05）（WKY：118 ± 8 mmHg，n = 5；SHR：185 ± 9 mmHg，n = 5）。SHR的心脏重量也显著增加（P < 0.05）（SHR的干心脏重量与体重之比为0.73 ± 0.04，n = 5；WKY为0.55 ± 0.02，n = 5）。使用位移试剂辅助和三量子滤波（TQF）核磁共振技术测量的细胞内钠水平，与正常血压大鼠心脏（8.4 ± 2.3 mmol/L，n = 5）相比，在离体Langendorff灌注的高血压大鼠心脏中显著升高（P < 0.05）（17.3 ± 3.6 mmol/L，n = 5）。这些数据表明原发性高血压中心肌钠含量增加。我们还研究了起搏对心脏TQF 23Na核磁共振的影响，发现WKY和SHR心脏在加快起搏时TQF Na+含量均增加。这些结果支持在生理Ca2+浓度下灌注的大鼠心脏中存在钠泵滞后现象，并表明高血压大鼠心脏已适应以补偿基础细胞内Na+增加并维持对心率增加的正常反应。我们的数据似乎表明离子对大鼠遗传性高血压的心肌肥大有贡献。
