DiBona Gerald F, Jones Susan Y
Department of Internal Medicine, University of Iowa College of Medicine and Veterans Administration Medical Center, Iowa City, IA 52242, USA.
J Hypertens. 2003 Aug;21(8):1539-46. doi: 10.1097/00004872-200308000-00019.
To study effects of endogenous angiotensin II on responses to standardized stimulation of afferent neural input into the central portion of the arterial and cardiac baroreflexes.
Different dietary sodium intakes were used to physiologically alter endogenous angiotensin II activity. Candesartan, an angiotensin II type 1 receptor antagonist, was used to assess dependency of observed effects on angiotensin II stimulation of angiotensin II type 1 receptors. Electrical stimulation of arterial and cardiac baroreflex afferent nerves was used to provide a standardized input to the central portion of the arterial and cardiac baroreflexes.
In anesthetized rats in balance on low, normal and high dietary sodium intake, arterial pressure, heart rate and renal sympathetic nerve activity responses to electrical stimulation of vagus and aortic depressor nerves were determined. Compared with plasma renin activity values in normal dietary sodium intake rats, those from low dietary sodium intake rats were higher and those from high dietary sodium intake rats were lower. During vagus nerve stimulation, the heart rate, arterial pressure and renal sympathetic nerve activity responses were similar in all three dietary sodium intake groups. During aortic depressor nerve stimulation, the heart rate and arterial pressure responses were similar in all three dietary sodium intake groups. However, the renal sympathetic nerve activity response was significantly greater in the low sodium group than in the normal and high sodium group at 4, 8 and 16 Hz. Candesartan administered to low dietary sodium intake rats had no effect on the heart rate and arterial pressure responses to either vagus or aortic depressor nerve stimulation but increased the magnitude of the renal sympathoinhibitory responses.
Increased endogenous angiotensin II in rats on a low dietary sodium intake attenuates the renal sympathoinhibitory response to activation of the cardiac and sinoaortic baroreflexes by standardized vagus and aortic depressor nerve stimulation, respectively.
研究内源性血管紧张素II对动脉和心脏压力反射中枢部分传入神经输入标准化刺激反应的影响。
采用不同的饮食钠摄入量来生理改变内源性血管紧张素II活性。使用坎地沙坦,一种血管紧张素II 1型受体拮抗剂,来评估观察到的效应是否依赖于血管紧张素II对血管紧张素II 1型受体的刺激。通过电刺激动脉和心脏压力反射传入神经,为动脉和心脏压力反射中枢部分提供标准化输入。
在低、正常和高饮食钠摄入量平衡的麻醉大鼠中,测定对迷走神经和主动脉减压神经电刺激的动脉血压、心率和肾交感神经活动反应。与正常饮食钠摄入大鼠的血浆肾素活性值相比,低饮食钠摄入大鼠的血浆肾素活性值较高,高饮食钠摄入大鼠的血浆肾素活性值较低。在迷走神经刺激期间,三个饮食钠摄入组的心率、动脉血压和肾交感神经活动反应相似。在主动脉减压神经刺激期间,三个饮食钠摄入组的心率和动脉血压反应相似。然而,在4、8和16Hz时,低钠组的肾交感神经活动反应明显大于正常和高钠组。给低饮食钠摄入大鼠施用坎地沙坦对迷走神经或主动脉减压神经刺激的心率和动脉血压反应没有影响,但增加了肾交感抑制反应的幅度。
低饮食钠摄入大鼠内源性血管紧张素II增加,分别减弱了对标准化迷走神经和主动脉减压神经刺激激活心脏和窦主动脉压力反射的肾交感抑制反应。