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Am J Physiol Heart Circ Physiol 286: H1706–H1711, 2004;
10.1152/ajpheart.01097.2003.
Cardiac sympathetic afferent stimulation impairs baroreflex control of renal
sympathetic nerve activity in rats
Lie Gao, Zhen Zhu, Irving H. Zucker, and Wei Wang
Department of Physiology and Biophysics, Nebraska Medical Center, University
of Nebraska College of Medicine, Omaha, Nebraska 68198-4575
Submitted 1 December 2003; accepted in final form 4 January 2004
angiotensin type 1 receptor
THE ARTERIAL BARORECEPTOR REFLEX plays an important role in
the adaptation and regulation of blood pressure in both physiological and pathophysiological situations (8). Despite the
many advances made toward understanding arterial baroreflex
reflex function, very little is known concerning how the baroreflex is regulated by other cardiovascular reflexes.
Our previous study showed that in the chronic heart failure
(CHF) state, not only is the arterial baroreflex gain depressed
(17, 18, 25, 26) but also the cardiac sympathetic afferent reflex
gain is significantly enhanced (24, 28, 29). The cardiac sympathetic afferent reflex is a sympathoexcitatory reflex (12) and
may contribute to the increase of sympathetic outflow in CHF
(27). On the other hand, many studies (2, 6, 10, 23, 31) have
solidly supported the idea that sympathetic activity can antagonize arterial baroreflex function in both humans and experi-
Address for reprint requests and other correspondence: W. Wang, Dept. of
Physiology and Biophysics, Univ. of Nebraska Medical Center, 984575 Nebraska Medical Center, Omaha, NE 68198-4575 (E-mail: weiwang
@unmc.edu).
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mental animals. Chemical sympathectomy markedly potentiates the baroreceptor reflex in normal rats (5) and prevents the
occurrence of the baroreceptor reflex impairment associated
with chronic heart failure (15). We thus reasoned that because
the cardiac sympathetic afferent reflex contributes to an increase in sympathetic outflow, this enhanced sympathetic activity may antagonize baroreflex function. If the cardiac sympathetic afferent reflex is augmented in CHF, this may be
responsible for the suppressed arterial baroreceptor reflex associated with CHF. Thus it can be hypothesized that in normal
rats, chemical and electrical stimulation of the cardiac sympathetic afferent reflex results in an increase in sympathetic nerve
activity, followed by a decrease in the gain of arterial baroreflex. Therefore, the first goal of this study was to determine
whether the chemical and electrical stimulation of cardiac
sympathetic afferents impairs arterial baroreflex function in
normal rats.
It has been shown that the renin-angiotensin (ANG) system
is activated in human and experimental chronic heart failure
(13, 33). Central ANG II plays an important role in both
depressing the arterial baroreceptor reflex (33) and in enhancing the cardiac sympathetic afferent reflex associated with the
CHF state (27). Blockade of the ANG II type 1 receptor in
CHF animals not only normalized the enhanced cardiac sympathetic afferent reflex (11) and reduced sympathetic tone (4)
but also restored the impaired arterial baroreflex function (16).
Given the above-mentioned close relationship between the
renin-ANG II system, arterial baroreflex, and cardiac sympathetic afferent reflex, the second goal of the present study was
to test the hypothesis that the central ANG II mechanism is
involved in the effect of electrical stimulation of cardiac
sympathetic afferent stimulation on arterial baroreceptor reflex
function in normal rats.
METHODS
Male Sprague-Dawley rats weighing between 350 and 420 g were
used in these experiments. All experiments were approved by the
Institutional Animal Care and Use Committee of the University of
Nebraska Medical Center and were carried out under the guidelines of
the American Physiological Society and the National Institutes of
Health Guide for the Care and Use of Laboratory Animals.
Each rat was anesthetized with urethane (800 mg/kg ip) and
␣-chloralose (40 mg/kg ip). Supplemental doses of anesthesia were
administered at 1/10 of the initial dose per hour. Body temperature
was maintained with the use of a heating pad. A midline incision in
the neck was made, and the trachea was cannulated to facilitate
mechanical ventilation. Through the midline incision in the neck, the
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0363-6135/04 $5.00 Copyright © 2004 the American Physiological Society
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Gao, Lie, Zhen Zhu, Irving H. Zucker, and Wei Wang. Cardiac
sympathetic afferent stimulation impairs baroreflex control of renal
sympathetic nerve activity in rats. Am J Physiol Heart Circ Physiol
286: H1706–H1711, 2004;10.1152/ajpheart.01097.2003.—It is well
known that cardiac sympathetic afferent reflexes contribute to increases in sympathetic outflow and that sympathetic activity can
antagonize arterial baroreflex function. In this study, we tested the
hypothesis that in normal rats, chemical and electrical stimulation of
cardiac sympathetic afferents results in a decrease in the arterial
baroreflex function by increasing sympathetic nerve activity. Under
␣-chloralose (40 mg/kg) and urethane (800 mg/kg ip) anesthesia, renal
sympathetic nerve activity, mean arterial pressure, and heart rate were
recorded. The arterial baroreceptor reflex was evaluated by infusion of
nitroglycerin (25 ␮g iv) and phenylephrine (10 ␮g iv). Left ventricular
epicardial application of capsaicin (0.4 ␮g in 2 ␮l) blunted arterial
baroreflex function by 46% (maximum slope 3.5 ⫾ 0.3 to 1.9 ⫾
0.2%/mmHg, P ⬍ 0.01). When the central end of the left cardiac
sympathetic nerve was electrically stimulated (7 V, 1 ms, 20 Hz), the
sensitivity of the arterial baroreflex was similarly decreased by 42%
(maximum slope 3.2 ⫾ 0.3 to 1.9 ⫾ 0.4%/mmHg; P ⬍ 0.05).
Pretreatment with intracerebroventricular injection of losartan (500
nmol in 1 ␮l of artificial cerebrospinal fluid) completely prevented the
impairment of arterial baroreflex function induced by electrical stimulation of the central end of the left cardiac sympathetic nerve
(maximum slope 3.6 ⫾ 0.4 to 3.1 ⫾ 0.5%/mmHg). These results
suggest that the both chemical and electrical stimulation of the cardiac
sympathetic afferents reduces arterial baroreflex sensitivity and the
impairment of arterial baroreflex function induced by cardiac sympathetic afferent stimulation is mediated by central angiotensin type 1
receptors.
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CARDIAC SYMPATHETIC AFFERENTS BLUNTS BAROREFLEX
AJP-Heart Circ Physiol • VOL
All values are expressed as means ⫾ SE. We constructed composite baroreflex curves by averaging the four parameters of the logistic
equation for all curves and using the mean parameters to construct a
single curve. Data were analyzed with a paired t-test when comparing
effects of capsaicin, electrical stimulation, and losartan in each group.
A value of P ⬍ 0.05 was considered statistically significant.
RESULTS
Effects of epicardial application of capsaicin on arterial
baroreflex function. Table 1 shows the effects of epicardial
application of capsaicin on MAP, HR, RSNA, and several
baroreflex curve parameters. Although there were no significant differences in HR, MAP and RSNA were significantly
higher during application of capsaicin compared with baseline.
Whereas capsaicin had no significant effects on the range of
RSNA response, BP50, and minimum RSNA, it did reduce the
average slope and Gainmax of the arterial baroreflex curve.
Figure 1 shows an original recording of arterial blood
pressure changes induced by phenylephrine after the injection
of nitroglycerin and attendant RSNA reflex responses before
and during epicardial application of capsaicin in one rat. It is
evident that the reflex RSNA response to phenylephrine is
virtually absent during epicardial application of capsaicin. The
group data shown in Fig. 2 indicates a significant attenuation of
the Gainmax during stimulation of the cardiac sympathetic
afferent nerve.
Effects of electrical cardiac sympathetic afferent stimulation
on arterial baroreflex function. Table 2 shows the effects of
electrical cardiac sympathetic afferent stimulation on MAP,
HR, RSNA, and several of the baroreflex curve parameters. As
shown in Table 2, there were no significant differences in HR
levels; however, MAP and RSNA were significantly higher
during electrical stimulation of cardiac sympathetic afferents
compared with compared with baseline. Electrical stimulation
of cardiac sympathetic afferents had no significant effects on
the range of RSNA response, BP50, or minimum RSNA, but it
reduced the average slope and Gainmax of the arterial baroreflex curve.
Figure 3 shows an original recording of arterial blood
pressure changes induced by phenylephrine injection after the
injection of nitroglycerin and attendant RSNA reflex responses
before and during electrical stimulation of cardiac sympathetic
afferents in one rat. As seen for chemical stimulation, it is
evident that the reflex RSNA response to phenylephrine is
almost completely absent during electrical stimulation. This
Table 1. Effect of epicardial application of capsaicin on
MAP, HR, RSNA, and baroreflex parameters
Parameter
Control
Capsaicin
MAP, mmHg
HR, beats/min
RSNA, %
Range of RSNA response, %
Average slope, %/mmHg
BP50, mmHg
Minimum RSNA, %
Gainmax, %/mmHg
90.3⫾5.5
325.2⫾12.1
100
107.4⫾12.4
0.13⫾0.03
90.1⫾10.7
25.9⫾3.7
3.5⫾0.3
105.4⫾4.9*
327.9⫾15.8
178.7⫾17.6†
102.9⫾9.9
0.07⫾0.01*
89.3⫾10.5
26.3⫾5.4
1.9⫾0.2†
Values are means ⫾ SE; n ⫽ 12 rats. MAP, mean arterial pressure; HR,
heart rate; RSNA, renal sympathetic nerve activity; BP50, midpoint of RSNA
blood pressure range; Gainmax, maximum gain. *P ⬍ 0.05, †P ⬍ 0.01
compared with the control.
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right common carotid artery was exposed and cannulated with a
catheter transducer (model SPR-524, Millar Instruments; Houston,
TX) for measurement of mean artery pressure (MAP). Heart rate (HR)
was derived from the arterial pressure pulse using a PowerLab model
16S (ADInstruments; Colorado Springs, CO). A femoral vein was
cannulated with a polyethylene-20 catheter for administration of
drugs.
Recording of renal sympathetic nerve activity. The left kidney,
renal artery, and nerves were exposed through a left retroperitoneal
flank incision. The renal sympathetic nerves were identified, dissected
free of the surrounding connective tissue, and was placed on a pair of
platinum-iridium recording electrodes. When an optimal signal-tonoise ratio was achieved, the electrode and the renal nerve were
covered with a fast setting silicone (Kwik-Sil, World Precision Instruments; Sarasota, FL). The signal was amplified with a Grass direct
current preamplifier (model P18D, Astro-Med; West Warwick, RI)
with the low-frequency cutoff set at 30 to 100 Hz and high-frequency
cutoff at 1 to 3 kHz. The amplified discharge was monitored on a
storage oscilloscope (model 121 N, Tektronix; Beaverton, OR) and
then imported to a computer system with other parameters. A voltage
integrator (model 1801, Buxco Electronics) was used for quantifying
the raw renal sympathetic nerve activity (RSNA). The raw nerve
activity, integrated nerve activity, arterial pressure, and HR were
recorded on a PowerLab data-acquisition system (model 16S, ADInstruments) and stored on disk until analyzed.
Epicardial application of capsaicin. The chest was opened through
the fourth intercostal space. The pericardium was removed to expose
the left ventricle. A piece of filter paper (3 ⫻ 3 mm) containing
capsaicin (0.4 ␮g in 2 ␮l) was applied to the epicardial surface of the
anterior surface of the left ventricle. Each drug was applied for ⬃2
min until the end of the baroreflex test, and then the filter paper was
removed and the epicardium was rinsed three times with 10 ml of
warm normal saline (38°C).
Electrical stimulation of cardiac sympathetic afferents. The chest
was opened through the left second intercostal space. The left ventral
ansa, which contains cardiac sympathetic afferent nerves, was identified, tied, and ligated. A pair of stainless steel stimulation electrodes
was placed on the central end of this nerve. The stimulus (7 V, 1 ms,
20 Hz) was delivered with a stimulator (Grass S88, Astro-Med) and a
stimulus isolation unit until the end of each baroreflex test.
Intracerebroventricular losartan. The rats were placed in a stereotaxic head holder (Stoelting; Chicago, IL) and the skull was exposed
through an incision on the midline of the scalp. After the bregma was
identified, an intracerebroventricular cannula (outer diameter 0.5 mm
and inner diameter 0.1 mm) connected to a microsyringe (model 7001,
Hamilton; Reno, NV) was implanted into the right cerebral ventricle.
The coordinates were determined from the Paxinos and Watson rat
atlas (20), which were 0.8 mm posterior, 1.4 mm lateral to the bregma,
and 3.8 mm ventral to the zero level. Losartan (500 nmol in 1 ␮l of
artificial cerebrospinal fluid in 1 min) was infused. At the end of the
experiment, the cannula tip placement was confirmed by microinjection of fast green (1 ␮l).
Construction of arterial baroreflex curves and statistical analysis.
RSNA was expressed as the percent change from baseline. Baroreflex
curves were generated by measurement of RSNA responses to decreases and then increases in arterial pressure by intravenous infusions
of nitroglycerin (25 ␮g iv) and phenylephrine (10 ␮g iv). MAP was
altered at a rate of 1 mmHg/s during these infusions. The MAP data
were acquired every 2 s from the threshold to the saturation points. A
sigmoid logistic function was fit to the data using a nonlinear regression program (SigmaPlot version 8.0, SPSS; Chicago, IL) run on a
microcomputer. Four parameters were derived from the equation
%RSNA ⫽ A/{1 ⫹ exp [B (MAP ⫺ C)]} ⫹ D, where A is the RSNA
range, B is the slope coefficient, C is the pressure at the midpoint of
the RSNA range (BP50), and D is the minimum RSNA (7). The peak
slope [or maximum gain (Gainmax)] was determined by taking the first
derivative of the baroreflex curve described by the equation.
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CARDIAC SYMPATHETIC AFFERENTS BLUNTS BAROREFLEX
pattern was confirmed by the average group data shown in Fig.
4, in which the significantly blunted baroreflex slope is apparent during electrical stimulation.
Effects of intracerebroventricular losartan on baroreflex
function after electrical cardiac sympathetic afferent stimulation. Table 3 shows the effects of intracerebroventricular losartan (500 nmol in 1 ␮l artificial cerebrospinal fluid in 1 min)
on the response to electrical cardiac sympathetic afferent stimulation and baroreflex function. No significant differences in
HR, MAP, RSNA, or any of the baroreflex curve parameters
were observed after intracerebroventricular losartan compared
with baseline. However, intracerebroventricular losartan prevented electrical stimulation of cardiac sympathetic afferents
from enhancing MAP and RSNA and from lowering the
average slope and Gainmax of the arterial baroreflex function
(Fig. 5). Figure 6 shows the composite baroreflex curves
generated before and after intracerebroventricular losartan.
These curves are nearly superimposable and there were no
significant differences. The average Gainmax was 3.3 ⫾ 0.2%/
mmHg before losartan and 3.6 ⫾ 0.4%/mmHg after losartan.
Figure 7 shows the composite baroreflex curves generated
before and during cardiac sympathetic afferent electrical stimulation after intracerebroventricular losartan. These curves are
also nearly superimposable. The average maximum gain was
3.6 ⫾ 0.4%/mmHg before electrical stimulation and 3.1 ⫾
0.5%/mmHg after electrical stimulation.
DISCUSSION
The major new finding of our study is that, in anesthetized
rats, both left ventricular epicardial application of capsaicin
and electrical stimulation of left cardiac sympathetic afferents
impair the baroreflex control of RSNA mainly via reducing the
average slope and Gainmax of the arterial baroreflex curve. This
is the first time, to our knowledge, that it has been demonTable 2. Effect of electrical cardiac sympathetic
afferent stimulation on resting MAP, HR, RSNA,
and baroreflex parameters
Fig. 2. Composite arterial baroreflex curves generated before and during
epicardial application of capsaicin in normal rats (n ⫽ 12). Inset, gain curves
of these mean baroreflex curves. **P ⬍ 0.01 compared with before losartan.
AJP-Heart Circ Physiol • VOL
Parameter
Control
Electrical
Stimulation
MAP, mmHg
HR, beats/min
RSNA, %
Range of RSNA response, %
Average slope, %/mmHg
BP50, mmHg
Minimum RSNA, %
Gainmax, %/mmHg
91.3⫾6.1
326.4⫾11.5
100
105.7⫾9.6
0.12⫾0.05
93.3⫾11.3
37.3⫾5.5
3.2⫾0.3
109.4⫾7.5*
328.9⫾9.8
192.2⫾21.3†
108.7⫾12.3
0.07⫾0.01†
88.8⫾9.6
39.1⫾3.2
1.9⫾0.4*
Values are means ⫾ SE; n ⫽ 12 rats. *P ⬍ 0.05, †P ⬍ 0.01 compared with
control.
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Fig. 1. Original recording of arterial blood
pressure (ABP) changes induced by phenylephrine injection (10 ␮g iv) and attendant
renal sympathetic nerve activity (RSNA) reflex responses in a rat before (A) or during
(B) epicardial application of capsaicin (0.4
␮g in 2 ␮l). Note the suppressed reflex
RSNA response to phenylephrine during
epicardial application of capsaicin. MAP,
mean arterial pressure.
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CARDIAC SYMPATHETIC AFFERENTS BLUNTS BAROREFLEX
strated that the chemically and electrically evoked cardiac
sympathetic afferent reflex inhibits arterial baroreflex function.
In addition, we found that pretreatment with intracerebroventricular losartan inhibits the response of electrical stimulation
of cardiac sympathetic afferents from suppressing baroreflex
control of RSNA. This indicates that the inhibition of baroreflex function by stimulation of the cardiac sympathetic afferent
reflex is mediated by central ANG type 1 receptors.
Sympathetic nerves innervating the heart contain sensory
fibers, which enter the spinal cord via upper thoracic dorsal
roots (19). Various substances that may be augmented in the
myocardium during ischemia excite these nerve endings (1,
22). It has been suggested that cardiac sympathetic afferent
nerves contribute to reflex control of the circulation via spinal
and supraspinal pathways in physiological and certain patho-
logical conditions (12). In the present study, during application
of capsaicin to the left ventricle or electrical stimulation of the
left cardiac sympathetic afferent nerves, we observed sympathoexcitation and the subsequent elevation in MAP. This was
essentially similar to previous studies using rats and dogs (29,
32). It is notable that the elevated MAP occurs subsequent to
the increase in RSNA without an increase in HR, suggesting
that the change of MAP induced by evoked cardiac sympathetic afferent reflex in this study was primarily due to a change
in peripheral resistance.
It is now well accepted that the cardiac sympathetic afferent
reflex is augmented (24, 28, 29) and the arterial baroreflex is
depressed (17, 18, 25, 26) in the CHF state. However, it is not
clear what, if any, relationship exists between these two cardiovascular reflexes. Because the cardiac sympathetic afferent
reflex is a sympathoexcitatory reflex (12) and contributes to the
elevation in sympathetic tone (27), which antagonizes arterial
baroreflex function (2, 6, 10, 23, 31), it is possible that the
Table 3. Effect of electrical cardiac sympathetic afferent
stimulation on resting MAP, HR, RSNA, and baroreflex
parameters after icv losartan in normal rats
Fig. 4. Composite arterial baroreflex curves generated before and during
electrical stimulation of cardiac sympathetic afferent in normal rats (n ⫽ 12).
Inset, gain curves of these mean baroreflex curves. *P ⬍ 0.05 compared with
before stimulation.
AJP-Heart Circ Physiol • VOL
Parameter
Control
Losartan
Electrical
Stimulation ⫹
Losartan
MAP, mmHg
HR, beats/min
RSNA, %
Range of RSNA response, %
Average slope, %/mmHg
BP50, mmHg
Minimum RSNA, %
Gainmax, %/mmHg
93.7⫾10.2
331.6⫾13.6
100
106.6⫾13.4
0.13⫾0.05
88.6⫾9.7
27.2⫾4.3
3.3⫾0.2
90.2⫾7.6
326.3⫾17.5
96.6⫾7.5
110.3⫾9.9
0.13⫾0.04
94.2⫾11.3
23.3⫾4.2
3.6⫾0.4
92.7⫾8.3*
329.4⫾15.3
99.4⫾6.2†
106.7⫾8.5
0.12⫾0.02†
91.3⫾10.1
26.7⫾4.5
3.1⫾0.5†
Values are means ⫾ SE. icv, intracerebroventricular. *P ⬍ 0.05, †P ⬍ 0.01
compared with values of electrical stimulation of cardiac sympathetic afferent
without icv losartan.
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Fig. 3. Original recording of ABP changes
induced by phenylephrine injection (10 ␮g
iv) and attendant RSNA reflex responses in a
rat before (A) or during (B) electrical stimulation (7 V, 1 ms, 20 Hz) of cardiac sympathetic afferents. Note the suppressed reflex
RSNA silence response to phenylephrine
during electrical stimulation.
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CARDIAC SYMPATHETIC AFFERENTS BLUNTS BAROREFLEX
augmented cardiac sympathetic afferent reflex impairs arterial
baroreflex function in CHF via its sympathoexcitatory effects.
The results of this study imply a central interaction between the
cardiac sympathetic afferent reflex and the arterial baroreflex.
This interaction may be of profound importance in the CHF
state as well as in other abnormalities in which this reflex is
evoked such as during coronary ischemia.
The exact mechanism(s) by which arterial baroreflex function is impaired by stimulation of the cardiac sympathetic
afferent reflex are not clear. However, it is well known that
ANG II modulates sympathetic function at many loci in the
central nervous systems (14, 30). ANG II has been shown to
augment sympathetic outflow in various portions of the hypothalamus and medulla (21, 33). It has also been shown that
central administration of losartan reduced RSNA and restored
baroreflex sensitivity in rats with chronic myocardial infarc-
Fig. 6. Composite arterial baroreflex curves generated before and after intracerebroventricular losartan in normal rats (n ⫽ 12). Inset, gain curves of these
mean baroreflex curves.
AJP-Heart Circ Physiol • VOL
tion-induced CHF (4), indicating that blockade of a central
ANG II mechanism reduced sympathetic tone and enhanced
arterial baroreflex function (9). On the other hand, our studies
have shown that central administration of losartan normalized
the enhanced cardiac sympathetic afferent reflex in dogs with
pacing-induced CHF (11). The findings in the present study
showed that intracerebroventricular administration of losartan
normalized the enhanced RSNA induced by electrical stimulation of cardiac sympathetic afferents and prevented it from
impairing arterial baroreflex function, strongly suggesting that
central ANG II mediates the renal sympathetic response, at
least, to electrical stimulation of cardiac sympathetic afferent
stimulation. Although ANG II may modulate sympathetic
function in the central and the peripheral nervous systems (21),
and losartan might pass the blood-brain barrier, it is unlikely
Fig. 7. Composite arterial baroreflex curves generated before and during
electrical stimulation of cardiac sympathetic afferent with pretreatment of
intracerebroventricular losartan (n ⫽ 12). Inset, gain curves of these mean
baroreflex curves.
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Fig. 5. Pretreatment with intracerebroventricular losartan abolishes the effects of electrical cardiac sympathetic afferent stimulation on MAP (A), RSNA (B), and arterial
baroreflex function (C and D). *P ⬍ 0.05,
**P ⬍ 0.01 compared with before losartan,
n ⫽ 12.
CARDIAC SYMPATHETIC AFFERENTS BLUNTS BAROREFLEX
GRANTS
This study was supported by an American Heart Association grant-in-aid
and National Heart, Lung, and Blood Institute Grant PO1-HL-62222.
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that the effect of intracerebroventricular administration of losartan in the present study was due to a peripheral action of
losartan because our previous study indicated that intravenous
administration of the same dose of losartan significantly decreased baseline MAP, which did not occur in the present
study. Furthermore, administration of the same dose of losartan
intravenously has no effect on the cardiac sympathetic afferent
reflex sensitivity (32).
Our previous finding (32) showed that intracerebroventricular administration of losartan normalized the enhanced cardiac sympathetic afferent reflex evoked by epicardial application of both bradykinin and capsaicin in rats with CHF, but had
no significant effects on the cardiac sympathetic afferent reflex
in sham rats. However, in the present study we found that
intracerebroventricular administration of losartan prevented the
electrical stimulation of cardiac sympathetic afferents from
increasing RSNA and elevating MAP in normal rats. The
reason for these differences may be related to the method used
to evoke the cardiac sympathetic afferent reflex or the preparation of the animals. In our previous experiment, we used the
epicardial application of bradykinin and capsaicin to evoke the
cardiac sympathetic afferent reflex, which may be involved in
both sympathetic and parasympathetic components (3). In
addition, the animals we used in that experiment were sinoaortic denervated, which might have an influence on the
magnitude of the response to stimulation of cardiac sympathetic afferents.
In summary, the present results show that chemical and
electrical stimulation of the cardiac sympathetic afferent reflex
reduces arterial baroreflex control of RSNA in anesthetized
normal rats and that this effect is mediated by a central ANG
II mechanism. The results observed in this study provide new
insight and a possible explanation for the blunted arterial
baroreflex function in CHF, a condition in which the cardiac
sympathetic afferent reflex is markedly enhanced.
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