DiBona G F, Jones S Y, Sawin L L
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52240, USA.
Am J Physiol. 1996 Aug;271(2 Pt 2):R361-7. doi: 10.1152/ajpregu.1996.271.2.R361.
To determine the effects of physiological alterations in endogenous angiotensin II (ANG II) activity on basal renal sympathetic nerve activity and its arterial baroreflex regulation, the effect of ANG II receptor (AT1) blockade with losartan was examined in conscious rats consuming low, normal, or high sodium diet that were instrumented for the simultaneous measurement of arterial pressure and renal sympathetic nerve activity. Intravenous losartan decreased arterial pressure in low (-27 +/- 4 mmHg) and normal (-15 +/- 2 mmHg) but not in high sodium diet rats (-5 +/- 2 mmHg). When arterial pressure had been restored to the prelosartan value with methoxamine infusion, renal sympathetic nerve activity was decreased in low (-27 +/- 4%) and normal (-20 +/- 3%) but not in high sodium diet rats (-5 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-8 +/- 2 mmHg) and normal (-7 +/- 2 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). Intracerebroventricular losartan did not significantly decrease arterial pressure but decreased renal sympathetic nerve activity in low (-28 +/- 5%) and normal (-20 +/- 4%) but not in high sodium diet rats (-2 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-7 +/- 2 mmHg) and normal (-5 +/- 1 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). These results indicate that physiological alterations in endogenous ANG II activity tonically influence basal levels of renal sympathetic nerve activity and its arterial baroreflex regulation.
为了确定内源性血管紧张素II(ANG II)活性的生理改变对基础肾交感神经活性及其动脉压力反射调节的影响,我们在食用低、正常或高钠饮食的清醒大鼠中检测了氯沙坦对ANG II受体(AT1)的阻断作用,这些大鼠已安装仪器以同时测量动脉血压和肾交感神经活性。静脉注射氯沙坦可降低低钠(-27±4 mmHg)和正常钠(-15±2 mmHg)饮食大鼠的动脉血压,但对高钠饮食大鼠(-5±2 mmHg)无效。当通过甲氧明输注使动脉血压恢复到氯沙坦给药前的值时,低钠(-27±4%)和正常钠(-20±3%)饮食大鼠的肾交感神经活性降低,但高钠饮食大鼠(-5±2%)未降低。低钠(-8±2 mmHg)和正常钠(-7±2 mmHg)饮食大鼠的肾交感神经活性的动脉压力反射调节移向较低压力(动脉血压处于中值),但高钠饮食大鼠(0±2 mmHg)未出现这种情况。脑室内注射氯沙坦未显著降低动脉血压,但可降低低钠(-28±5%)和正常钠(-20±4%)饮食大鼠的肾交感神经活性,而高钠饮食大鼠(-2±2%)未降低。低钠(-7±2 mmHg)和正常钠(-5±1 mmHg)饮食大鼠的肾交感神经活性的动脉压力反射调节移向较低压力(动脉血压处于中值),但高钠饮食大鼠(0±2 mmHg)未出现这种情况。这些结果表明,内源性ANG II活性的生理改变对肾交感神经活性的基础水平及其动脉压力反射调节具有持续性影响。