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Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575
The aims of present study were to
determine whether angiotensin II (ANG II) in the paraventricular
nucleus (PVN) is involved in the central integration of the cardiac
sympathetic afferent reflex and whether this effect is mediated by the
ANG type 1 (AT1) receptor. While the animals were under
-chloralose and urethane anesthesia, mean arterial pressure, heart
rate, and renal sympathetic nerve activity (RSNA) were recorded in
sinoaortic-denervated and cervical-vagotomized rats. A cannula was
inserted into the left PVN for microinjection of ANG II. The cardiac
sympathetic afferent reflex was tested by electrical stimulation (5, 10, 20, and 30 Hz in 10 V and 1 ms) of the afferent cardiac sympathetic
nerves or epicardial application of bradykinin (BK) (0.04 and 0.4 µg in 2 µl). Microinjection of ANG II (0.03, 0.3, and 3 nmol) into the
PVN resulted in dose-related increases in the RSNA responses to
electrical stimulation. The percent change of RSNA response to 20- and
30-Hz stimulation increased significantly at the highest dose of ANG II
(3 nmol). The effects of ANG II were prevented by pretreatment with
losartan (50 nmol) into the PVN. Microinjection of ANG II (0.3 nmol)
into the PVN significantly enhanced the RSNA responses to epicardial
application of BK, which was abolished by pretreatment with losartan
(50 nmol) into the PVN. These results suggest that exogenous ANG II in
the PVN augments the cardiac sympathetic afferent reflex evoked by both
electrical stimulation of cardiac sympathetic afferent nerves and
epicardial application of BK. These central effects of ANG II are
mediated by AT1 receptors.
renal sympathetic nerve activity; angiotensin type 1 receptor
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