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-estradiol on the baroreflex control of
sympathetic activity in conscious ovariectomized rats
Department of Physiology, University of Tennessee, Memphis, Memphis, Tennessee 38163
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The effects of chronic treatment with
17
-estradiol on baroreflex control of sympathetic activity were
examined in conscious unrestrained ovariectomized rats. Baroreflex
function was evaluated by logistic sigmoidal analysis of the
relationships between changes in mean arterial pressure (MABP) and
changes in heart rate (HR) and splanchnic nerve activity (SNA) when
MABP was rapidly increased to 150 mmHg by intravenous phenylephrine
after its reduction to 50 mmHg by intravenous nitroprusside. These
baroreflex function curves were similar in vehicle- and
estradiol-treated rats. However, after a 30-min infusion of vasopressin
in vehicle-treated rats, the curve for HR was shifted downward, and the
upper plateau and maximum gain for the SNA curve were reduced. These
effects were abolished by estradiol. A 30-min phenylephrine infusion
had no effect on the baroreflex curves. Thus estrogen can modulate the action of vasopressin on baroreflex control of sympathetic outflow and
thereby participate in cardiovascular regulation.
blood pressure; heart rate; splanchnic nerve; vasopressin
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THERE IS EXPERIMENTAL evidence suggesting that estrogen
can affect cardiovascular function via actions directly on blood
vessels and on the autonomic nervous system. With respect to the
latter, estrogen receptors have been identified in brain centers
involved in cardiovascular regulation, e.g., the preoptic area, the
paraventricular and supraoptic nuclei, the nucleus of the solitary
tract (NTS), the ventrolateral medulla (VLM), and the area postrema
(AP) (25, 27). Since NTS, VLM, and AP are central nervous system
elements in the baroreceptor reflex arc, the location of estrogen
receptors in these areas suggests that estrogen may influence
baroreflex function. In support of this hypothesis, Akaishi and Homma
(2) recently reported that the responses of supraoptic vasopressin neurons to changes in blood pressure induced by intravenous injection of phenylephrine or nitroprusside were modified by estrogen in ovariectomized rats. Circulating vasopressin (AVP) can alter baroreflex activity via V1 receptors in the
AP (12). This effect requires 
2-adrenergic signaling within
the NTS (13). Because estrogen receptors exist in both the AP and
noradrenergic neurons of the NTS (27), estrogen may influence the
effect of AVP on the baroreflex.
The aim of the present study was to test the effects of estrogen and interactions between estrogen and AVP on baroreflex control of sympathetic activity in conscious ovariectomized rats.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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All experimental procedures were approved by the Institutional Animal Care and Use Committee and were conducted in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.
Animal preparation. The experiments
were carried out in 11- to 16-wk-old female Sprague-Dawley rats. They
were housed individually with free access to food and tap water in a
room with controlled temperature (24°C) and lighting (14:10-h
light-dark cycle). The rats were ovariectomized under ether 11 days
before the experiment. One week after ovariectomy, one group of rats,
under ether anesthesia, was given subcutaneous implants of Silastic
capsules containing 15 µg of 17-estradiol
each. The capsules were prepared by filling a 30-mm length
of Silastic tubing (1.98 mm ID and 3.18 mm OD) with 60 µl of a
solution of 17-estradiol dissolved in sesame oil (250 µg/ml).
After sealing the ends with Silastic to provide a 20-mm capsule
containing the estradiol, the capsules were incubated in 0.9% NaCl
overnight at 37°C before implantation in the rat to prevent a
transitory peak in the plasma estradiol concentration that would
otherwise occur. This procedure provides a stable plasma concentration
of estrogen similar to that at the time of the proestrous peak (34).
Control rats were implanted with similarly prepared Silastic capsules
containing only sesame oil.
Three days after implanting the capsules, the rats were anesthetized with Brevital (60 mg/kg ip). Anesthesia was maintained by supplemental intravenous Brevital as needed. Both femoral veins were catheterized with PE-10 tubing, and the right femoral artery was catheterized with PE-50 tubing. The left splanchnic nerve trunk was exposed via a left flank incision. A 2- to 3-mm length of the nerve was isolated from the connective tissue and placed on a bipolar silver wire electrode that was sutured to the surrounding tissue. The nerve was fixed on the electrode with silicone rubber (Wacker SilGel 604) when an optimal recording was obtained. The incisions were then closed. The electrode cable and the vascular catheters were tunneled subcutaneously to the back, where they exited. After surgery, the rat was allowed to wake up from anesthesia, usually within 30 min, and put in a cage (20 × 22 × 18 cm; width × depth × height) in which the rat could move freely. The catheters and cable were protected by a spring. Food and tap water ad libitum and 20 ml of 5% dextrose as drinking fluid were provided.
Twenty-four hours later the experiment was carried out while the rat was conscious and freely moving in the same cage. During the experiment, food and water were removed from the cage. The splanchnic nerve signals were amplified by a Gould Universal Amplifier with a band-pass filter (low 100 Hz; high 1,000 Hz). A MacLab data acquisition system with a sampling rate of 2,000/s was used to record the raw nerve signal; the signal was integrated over 1-s intervals, and mean (MABP) and phasic arterial blood pressure and heart rate (HR) were recorded. Nonbiological noise was obtained by recording from the nerve after death and was subtracted from the nerve signals recorded during the experiment.
Experimental protocol. Dynamic
baroreflex function curves were constructed to evaluate the effects of
estradiol on the baroreflex control of HR and splanchnic nerve activity
(SNA). Before challenging arterial blood pressure with sodium
nitroprusside and phenylephrine to obtain the first set of dynamic
baroreflex curves, the rats were monitored for 30-60 min to ensure
that MABP, HR, and SNA had attained a steady state. The average of the
data obtained during the last 60 s of this period, immediately before
the first intravenous infusion of sodium nitroprusside, was used to
provide control levels of MABP, HR, and SNA for both the first and
second set of baroreflex curves. In rats treated
(n = 15) or untreated (n = 15) with estradiol, arterial
blood pressure was rapidly changed by intravenous injection of sodium
nitroprusside (50-100
µg · min
1 · kg1)
to lower MABP to 50-60 mmHg within 20 s and then by graded
intravenous infusion of phenylephrine (6-60
µg · min1 · kg1)
to elevate MABP to 150-160 mmHg within 100 s. The rate of increase in MABP was 1-2 mmHg/s. The 1-s averages of data obtained from the
simultaneously recorded MABP, HR, and SNA when MABP increased from
50-60 to 150-160 mmHg were fitted to sigmoidal four-parameter logistic curves by the program SigmaPlot for the Macintosh (Fig. 1) according to the equation
f(x) = [a/(1 
eb(xc))] d, where
a = the range in the changes of SNA or
HR; b = the slope coefficient; c = 
MABP at the maximum rate of change;
d = the lower plateau (the minimum SNA
or HR); x = MABP; and
f(x) = SNA (%control) or change in HR.
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The upper plateau (the maximum SNA or HR) was equal to
a d, and the maximum gain
(Gmax) was
equal to
a · b/4.
Thirty minutes after the recovery from these brief disturbances in
MABP, HR, and SNA, the rats were given a 30-min intravenous infusion of
AVP (6.1 ng · min1 · kg1;
n = 7 for estradiol treated or
control) or phenylephrine (6.1 µg · min1 · kg1;
n = 8 for estradiol treated or
control). Immediately after the conclusion of the 30-min infusions of
AVP or phenylephrine, a second set of dynamic baroreflex function
curves were constructed as described to evaluate the effects of the
preceding infusions of AVP and phenylephrine in estradiol-treated and
control rats on the dynamic baroreflex control of HR and SNA.
Statistical analysis. Baroreflex
function curves for HR and SNA were constructed for each rat by
four-parameter logistic analysis as described, and the equations for
the curves were obtained. From these equations, HR and %SNA were
calculated for each rat at each of 41 points for MABP, as indicated in
Figs. 2 and
3. These data points were then averaged
within each experimental group. The parameters for these curves were
also obtained as indicated for each rat and summarized in Tables
1 and 3.
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The data for SNA and HR were analyzed separately. Student's
t-tests were used to test whether
treatment with 17-estradiol compared with vehicle had a significant
effect on each of the variables presented in Tables 1 and
2. For the statistical analysis of the data
presented in Table 3, treatments were
applied factorially in a two-way arrangement of estradiol or vehicle
treatment and intravenous infusion of AVP or phenylephrine. For each
analysis, three preplanned contrasts were made in the context of ANOVA; these contrasts were 1) estradiol
against vehicle in the presence of AVP,
2) estradiol against vehicle in the
presence of phenylephrine, and 3)
vehicle in the presence of AVP against vehicle in the presence of
phenylephrine (28). Because the number of contrasts was equal to the
number of degrees of freedom for a two-way ANOVA, a significance level
of 0.05 was used.
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The groups of data used to construct the baroreflex curves shown in Figs. 2 and 3 were subjected to a two-way ANOVA to determine if there were statistically significant differences among them.
Data are presented in figures and tables as means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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A sample recording from one rat and the baroreflex curves constructed for HR and SNA are shown in Fig. 1.
Baseline MABP was slightly lower in the estradiol-treated rats (101 ± 1 mmHg) than in the vehicle-treated rats (107 ± 1 mmHg, P < 0.05), whereas HR was not different between the estradiol (422 ± 6 beats/min)- and vehicle-treated rats (424 ± 7 beats/min). Baroreflex function curves before the 30-min infusion of AVP or phenylephrine (Fig. 2) and their parameters (Table 1) were similar in both groups of rats.
The changes from the initial control levels in MABP, SNA, and HR by the end of 30-min infusion of either AVP or phenylephrine are shown in Table 2. The infusion of AVP and phenylephrine caused pressor responses that were significantly greater in the vehicle-treated than in the estradiol-treated rats (P < 0.05). These average differences were 6 mmHg for AVP and 13 mmHg for phenylephrine. SNA and HR were reduced in response to both infusions, but the inhibition of SNA when phenylephrine was infused was greater in the estradiol-treated rats (P < 0.05). Treatment with estradiol had no effect on the reduction in HR in response to either infusion or in the inhibition of SNA in response to AVP.
At the completion of the 30-min infusion of AVP or phenylephrine, we again obtained baroreflex function curves in response to rapid changes in MABP (Fig. 3). When the data used to construct the baroreflex curves shown in Fig. 3 were subjected to a two-way ANOVA, it was found that the relationships between changes in MABP and changes in HR or SNA were significantly different for vehicle-treated rats infused with AVP compared with estradiol-treated rats infused with AVP or with vehicle-treated rats infused with phenylephrine. The logistical parameters for these curves are summarized in Table 3. The upper plateau, range, and Gmax of the baroreflex curve for SNA were smaller (P < 0.05) in the vehicle-treated rats than in the estradiol-treated rats that had been infused with AVP. Moreover, the upper plateau and range of the baroreflex curve for SNA were smaller (P < 0.05) in the vehicle-treated rats that had been infused with AVP than in the vehicle-treated rats that had been infused with phenylephrine. Although, after the infusion of AVP, the upper and lower plateaus for HR were smaller in the vehicle-treated than in the estradiol-treated rats, these differences were not statistically significant. The upper plateau of the baroreflex curve for HR was smaller (P < 0.05) in the vehicle-treated rats after the infusion of AVP than after the infusion of phenylephrine. The logistical parameters for both HR and SNA were similar between the vehicle-treated and estradiol-treated rats that had been infused with phenylephrine.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The present experiments show that chronic treatment with estradiol had no effect on the dynamic baroreflex function curves when arterial blood pressure was changed rapidly. This result is different from our previous observation that estrogen had increased baroreflex sensitivity when there was a sustained increase in arterial pressure resulting from the intravenous infusion of phenylephrine (15). The mechanisms for these differential effects of estrogen on the baroreflex are uncertain, although it is well known that baroreflex function is influenced by the rate of change of arterial pressure (29). Seagard et al. (26) have reported that there are two types of carotid sinus baroreceptors that selectively contribute to "dynamic" or "tonic" baroreflex activity. Type I baroreceptors mainly contribute to dynamic baroreflex activity induced by rapid changes of blood pressure, whereas type II baroreceptors contribute to tonic baroreflex activity induced by sustained changes of blood pressure (26). The type I carotid baroreceptors project to a localized group of neurons in the dorsomedial subnucleus of the rostral NTS. In contrast, the type II baroreceptor afferents are more widely distributed to neurons in the commissural, medial, and dorsolateral subnuclei of the NTS (10). The selective effect of estrogen on tonic baroreflex function may relate to the differential pathways and function of these baroreceptor subtypes.
The present result is consistent with the report that chronic administration of estrogen did not change the baroreflex curve for renal sympathetic nerve activity in rabbits (4). However, chronic treatment with the combination of estrogen and progesterone increased the slope of the MABP-heart period relationship in ovariectomized ewes when blood pressure was challenged by a single dose of phenylephrine or nitroprusside (24). Because progesterone can modulate many physiological effects of estrogen and vice versa, that result is difficult to compare with the present study.
In untreated ovariectomized rats, intravenous infusion of AVP had profound effects on baroreflex function. When arterial pressure was changed rapidly, the entire baroreflex curve for HR was shifted downward and the upper plateau and maximum gain of the baroreflex function curve for SNA were reduced compared with these parameters in the rats treated with estradiol. It is unlikely that the differences in the effects of AVP on baroreflex function between the rats treated or untreated with estradiol were a result of the difference in the effect of intravenous infusion of AVP on MABP before the test of baroreflex function. The difference in the pressor response to phenylephrine between the untreated and estradiol-treated rats was even greater, but the baroreflex curves for HR and SNA were similar in these two groups of rats after phenylephrine infusion.
The effects of AVP on baroreflex function have been reported previously
(14, 21, 22, 32). Circulating AVP can activate neurons in the AP, which
is devoid of the blood-brain barrier, to facilitate the responses of
NTS neurons to afferent inputs (12). This effect of AVP requires
2-adrenergic signaling within the NTS (13). Estrogen receptors are located in both the AP and the
NTS. In the NTS, up to 60% of
2-noradrenergic neurons are
immunoreactive for the estrogen receptor (27), and transcriptional activity indicated by c-fos expression in these
neurons is affected by the estrous cycle or the administration of
estradiol (18). Consequently, the AP and the NTS are likely sites where
estrogen can act to interfere with the effects of circulating AVP on
the baroreflex. On other hand, circulating estrogen may also affect baroreceptor afferents (1, 11). Arterial baroreceptors are mechanosensitive nerve endings that are activated by deformation during
changes in arterial pressure. The activity of these receptors is
modulated by paracrine factors released from vascular endothelial cells. The activity of the baroreceptors is enhanced by prostacyclin (6, 35) and reduced by endothelin (5). It has been reported that
estrogen increases prostacyclin and decreases endothelin production in
vascular endothelium (3, 19, 20, 33). Thus it is also possible that
estrogen modulates the effect of AVP on baroreflex sensitivity
peripherally via these paracrine factors.
Perspectives
The effects of estrogen on baroreflex function and the sympathetic nervous system are likely to have important implications for cardiovascular regulation. They may contribute to the greater pressor responses to intravenous infusions of AVP (8) and phenylephrine (unpublished observations) in male rather than in nonestrous female rats, differences which are caused by estrogen (15, 31). Thus in the present experiments, the pressor responses to sustained infusions of vasopressin and phenylephrine were greater in vehicle-treated than in estrogen-treated rats, but the resulting inhibition of SNA was the same or greater in the estrogen-treated rats.In several experimental models of hypertension, e.g., deoxycorticosterone (DOC)-salt hypertension in the rat, the spontaneously hypertensive rat, and the Dahl salt-sensitive rat, the hypertension develops more rapidly in males than in females (9, 17, 23). It is possible that these gender differences may be caused in part by the effects of estrogen on the function of the sympathetic nervous system. Indeed, estrogen attenuates the development of hypertension in rats treated with DOC and salt (7) and in the spontaneously hypertensive rat (16), and baroreflex function is impaired in DOC-salt hypertension (30).
In the present study, we have also shown that estradiol can prevent the effects of AVP on baroreflex function in response to rapid changes in arterial pressure. The consequences of this interaction between estrogen and AVP for cardiovascular regulation will require further investigation.
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ACKNOWLEDGEMENTS |
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This research was supported by Grants 19209 and 12990 from the National Heart, Lung, and Blood Institute and by a grant from the Southern Research Consortium of the American Heart Association.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: L. Share, Dept. of Physiology, Univ. of Tennessee, Memphis, 894 Union Ave., Memphis, TN 38163 (E-mail: lshare{at}physio1.utmem.edu).
Received 3 August 1998; accepted in final form 27 April 1999.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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, 1-s averages of data. Solid lines are data fitted by
sigmoidal 4-parameter logistic analysis.
