Department of Cardiovascular Dynamics, Advanced Medical Engineering Center, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka, 565-8565, Japan.
J Physiol Sci. 2009 Nov;59(6):447-55. doi: 10.1007/s12576-009-0055-5. Epub 2009 Aug 18.
Although an acute arterial pressure (AP) elevation induced by intravenous angiotensin II (ANG II) does not inhibit sympathetic nerve activity (SNA) compared to an equivalent AP elevation induced by phenylephrine, there are conflicting reports as to how circulating ANG II affects the baroreflex control of SNA. Because most studies have estimated the baroreflex function under closed-loop conditions, differences in the rate of input pressure change and the magnitude of pulsatility may have biased the estimation results. We examined the effects of intravenous ANG II (10 microg kg(-1) h(-1)) on the open-loop system characteristics of the carotid sinus baroreflex in anesthetized and vagotomized rats. Carotid sinus pressure (CSP) was raised from 60 to 180 mmHg in increments of 20 mmHg every minute, and steady-state responses in systemic AP, splanchnic SNA and heart rate (HR) were analyzed using a four-parameter logistic function. ANG II significantly increased the minimum values of AP (67.6 +/- 4.6 vs. 101.4 +/- 10.9 mmHg, P < 0.01), SNA (33.3 +/- 5.4 vs. 56.5 +/- 11.5%, P < 0.05) and HR (391.1 +/- 13.7 vs. 417.4 +/- 11.5 beats/min, P < 0.01). ANG II, however, did not attenuate the response range for AP (56.2 +/- 7.2 vs. 49.7 +/- 6.2 mmHg), SNA (69.6 +/- 5.7 vs. 78.9 +/- 9.1%) or HR (41.7 +/- 5.1 vs. 51.2 +/- 3.8 beats/min). The maximum gain was not affected for AP (1.57 +/- 0.28 vs. 1.20 +/- 0.25), SNA (1.94 +/- 0.34 vs. 2.04 +/- 0.42%/mmHg) or HR (1.11 +/- 0.12 vs. 1.28 +/- 0.19 beats min(-1) mmHg(-1)). It is concluded that high levels of circulating ANG II did not attenuate the response range of open-loop carotid sinus baroreflex control for AP, SNA or HR in anesthetized and vagotomized rats.
尽管静脉内血管紧张素 II (ANG II) 引起的急性动脉压 (AP) 升高与苯肾上腺素引起的等效 AP 升高相比并不抑制交感神经活动 (SNA)，但关于循环 ANG II 如何影响压力反射控制 SNA 的报道却存在矛盾。由于大多数研究都是在闭环条件下估计压力反射功能，因此输入压力变化率和脉动幅度的差异可能会影响估计结果。我们在麻醉和迷走神经切断的大鼠中检查了静脉内 ANG II (10 microg kg(-1) h(-1)) 对颈动脉窦压力反射的开环系统特性的影响。颈动脉窦压力 (CSP) 每分钟增加 20 mmHg，从 60 增加到 180 mmHg，使用四参数逻辑函数分析系统 AP、内脏 SNA 和心率 (HR) 的稳态反应。ANG II 显著增加 AP 的最小值 (67.6 +/- 4.6 对 101.4 +/- 10.9 mmHg，P < 0.01)、SNA (33.3 +/- 5.4 对 56.5 +/- 11.5%，P < 0.05) 和 HR (391.1 +/- 13.7 对 417.4 +/- 11.5 次/分，P < 0.01)。然而，ANG II 并没有减弱 AP 的反应范围 (56.2 +/- 7.2 对 49.7 +/- 6.2 mmHg)、SNA (69.6 +/- 5.7 对 78.9 +/- 9.1%) 或 HR (41.7 +/- 5.1 对 51.2 +/- 3.8 次/分)。AP 的最大增益不受影响 (1.57 +/- 0.28 对 1.20 +/- 0.25)、SNA (1.94 +/- 0.34 对 2.04 +/- 0.42%/mmHg) 或 HR (1.11 +/- 0.12 对 1.28 +/- 0.19 次/分 min(-1) mmHg(-1))。结论是，在麻醉和迷走神经切断的大鼠中，循环中高水平的 ANG II 并没有减弱开环颈动脉窦压力反射控制 AP、SNA 或 HR 的反应范围。
