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Baroreflex Control of Sodium Excretion and Arterial Pressure
Department of Surgery, School of Medicine, University of Maryland, Baltimore, Maryland
Submitted 22 July 2004 ; accepted in final form 23 November 2004
We have developed a new model of chronic baroreceptor unloading (CBU) in the dog. Initial characterization of the model indicated that CBU increased mean arterial pressure (MAP) by an average of 22 mmHg for 7 days. The goal of the present study was to replicate the previous study using telemetry to record MAP continuously and to determine the effects of CBU (n = 7) on chronic regulation of MAP. We also prepared a group of dogs with sinoaortic denervation (SAD, n = 6) to compare the time course of changes in MAP in the two models. Control levels (7 day average ± SE) of MAP in the CBU and SAD groups were 94 ± 2 and 94 ± 1 mmHg, respectively. MAP averaged 124 ± 8 and 103 ± 4 mmHg during the first and second weeks after SAD (both P < 0.05) and then declined to levels not different from control during weeks 35. In the CBU group, MAP averaged 120 ± 4 mmHg during the first week, declined to 111 ± 4 mmHg during the second week, and stabilized at 104 mmHg during weeks 35 (all P < 0.05 compared with control). Plasma norepinephrine levels were increased significantly for the first week after SAD and for 2 wk after CBU but were not different from control for the remainder of the study. These results indicate that the initial increase in MAP after CBU is not sustained but declines to a level that is modestly higher than control. However, because MAP did not fall to control levels, the results are compatible with the hypothesis that baroreceptor input can influence the long-term level of MAP.
neurogenic hypertension; arterial baroreceptors; plasma norepinephrine; renin; aldosterone
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