High levels of circulating angiotensin II shift the open-loop baroreflex control of splanchnic sympathetic nerve activity, heart rate and arterial pressure in anesthetized rats

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.