Lacchini S, Ferlin E L, Moraes R S, Ribeiro J P, Irigoyen M C
Laboratory of Genetics and Molecular Cardiology, Hypertension Unit, Heart Institute (InCor), University of São Paulo, São Paulo, Brazil.
Hypertension. 2001 Sep;38(3):326-31. doi: 10.1161/hy0901.091179.
The aim of this study was to determine the contribution of NO to arterial pressure and heart rate variability in normotensive rats subjected to high sodium intake. Arterial pressure, heart rate, and arterial pressure and heart rate variability, baroreflex sensitivity, and pressure responsiveness were measured in male Wistar rats treated for 6 weeks (control and high sodium [1%] intake groups), before and after acute NO synthesis blockade. After treatment, no changes were observed in arterial pressure or heart rate. Arterial pressure variability was increased after sodium intake; however, heart rate variability and baroreflex sensitivity were not modified in high-sodium rats. NO synthase blockade increased arterial pressure in both groups but was higher in the high-sodium group (from 110+/-5 to 162+/-1.5 mm Hg) compared with the control group (from 109+/-6.7 to 144+/-10 mm Hg). The increase in arterial pressure was accompanied by a decrease in heart rate (from 354+/-28 to 303+/-25 bpm in control rats and from 380+/-34 to 298+/-30 bpm in high-sodium rats). NO synthase blockade increased the tachycardic response to sodium nitroprusside in high-sodium rats. Arterial pressure variability, evaluated by a nonlinear method (3D return maps), showed a larger reduction in response to NO synthase inhibition in the high-sodium group (from 162+/-26 to 34.8+/-8.6 for general index of beat-to-beat blood pressure variability) than in the control group (from 58+/-9.6 to 36+/-4.7 for general index of beat-to-beat blood pressure variability). Heart rate variability, evaluated by the SD of the R-R intervals, was not changed in control rats but was increased by NO synthase inhibition in the high-sodium rats (from 9.5+/-0.2 to 21.9+/-1.7 milliseconds). These findings suggest an important role for increased NO production in adaptation to high-sodium intake. The increase in NO system sensitivity in high-sodium intake may contribute to changes in the autonomic nervous system regulating heart rate and, especially, arterial pressure variability.
本研究的目的是确定一氧化氮（NO）对高钠摄入的正常血压大鼠动脉血压和心率变异性的影响。在雄性Wistar大鼠中，对其进行为期6周的治疗（分为对照组和高钠[1%]摄入组），在急性NO合成阻断前后，测量动脉血压、心率、动脉血压和心率变异性、压力反射敏感性以及压力反应性。治疗后，未观察到动脉血压或心率的变化。钠摄入后动脉血压变异性增加；然而，高钠大鼠的心率变异性和压力反射敏感性未发生改变。NO合酶阻断使两组的动脉血压均升高，但高钠组升高幅度更大（从110±5 mmHg升至162±1.5 mmHg），而对照组从109±6.7 mmHg升至144±10 mmHg。动脉血压升高伴随着心率下降（对照组大鼠从354±28次/分钟降至303±25次/分钟，高钠大鼠从380±34次/分钟降至298±30次/分钟）。NO合酶阻断增加了高钠大鼠对硝普钠的心动过速反应。通过非线性方法（三维返回映射）评估的动脉血压变异性显示，高钠组对NO合酶抑制的反应降低幅度更大（逐搏血压变异性总体指数从162±26降至34.8±8.6），而对照组（逐搏血压变异性总体指数从58±9.6降至36±4.7）。通过R-R间期标准差评估的心率变异性在对照组大鼠中未发生变化，但在高钠大鼠中，NO合酶抑制使其增加（从9.5±0.2毫秒增至21.9±1.7毫秒）。这些发现表明，增加的NO生成在适应高钠摄入中起重要作用。高钠摄入时NO系统敏感性的增加可能有助于调节心率的自主神经系统发生变化，并尤其有助于调节动脉血压变异性。
