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Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575
The aims of this
study were to determine whether ANG II is involved in the central
integration of the cardiac sympathetic afferent reflex (CSAR), and if
this central effect of ANG II is mediated by the
AT1 receptor. Experiments were
undertaken in dogs that were anesthetized with 
-chloralose,
sinoaortic denervated, and vagotomized. The renal sympathetic nerve
activity (RSNA) responses to varying frequency and voltage stimulation
of cardiac sympathetic afferent nerves were used to evaluate the
central sensitivity of the CSAR. In two groups of dogs, two doses (50 and 100 ng/min icv) of ANG II were acutely infused. In a
third group of dogs, ANG II was chronically infused for 3 days (100 ng/min, 1 µl/h icv). We found that acute infusion into the
cerebroventricle of two doses of ANG II did not affect the central
sensitivity of the CSAR or the baseline hemodynamics, but the baseline
RSNA increased significantly during the infusion of the higher dose of
ANG II. However, chronic intracerebroventricular infusion of ANG II
enhanced the central sensitivity of the CSAR significantly. In
addition, chronic intracerebrovetricular infusion of ANG II elicited a
significant increase in water intake and in arterial pressure from the
first and second day of infusion, respectively. In the group that
received chronic intracerebroventricular infusion of ANG II, the
administration of an AT1-receptor
antagonist losartan (0.125 mg/kg icv) abolished ANG II-induced
augmentation of the CSAR. These results suggest that chronic elevation
of central ANG II can sensitize the CSAR via central
AT1 receptors.
cerebroventricle; losartan; renal sympathetic nerve activity; chronic infusion; AT1 receptor
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