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-estradiol on sympathetic activity and pressor
response to phenylephrine in ovariectomized rats
Department of Physiology and Biophysics, University of Tennessee, 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 17
-estradiol
(E2) on sympathetic activity
were examined in conscious unrestrained ovariectomized rats,
instrumented under methohexital anesthesia to record mean arterial
pressure (MABP), heart rate (HR), renal nerve activity (RNA), and
splanchnic nerve activity (SNA) 1 day before the experiment. Injection
of E2 (150 µg/kg iv) caused
reductions (P < 0.01) in RNA (29 ± 6%), SNA (25 ± 2%), and HR (26 ± 5 beats/min) within 20 min, but MABP remained unchanged. Ninety minutes after intravenous
injection of E2 or vehicle,
intravenous infusion of phenylephrine (PE; 6.2 µg · min
1 · kg1)
induced similar increases in MABP and decreases in HR, RNA, and SNA in
both groups. By contrast, in rats chronically treated with
E2, the pressor response to PE was
smaller (P < 0.01; 22 ± 5 mmHg)
than in vehicle-treated rats (40 ± 4 mmHg). The changes in HR, RNA,
and SNA were similar in both groups, but the ratios of changes in HR
and SNA to MABP, an index of baroreflex sensitivity, were greater in
the E2-treated rats. These
findings suggest that E2 can act
centrally to modulate sympathetic function and thereby participate in
cardiovascular regulation.
blood pressure; renal nerve; splanchnic nerve; baroreflex
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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IT HAS BEEN AMPLY DEMONSTRATED that estrogen protects women against cardiovascular disease. Thus the incidence of cardiovascular disease is lower in premenopausal women than in age-matched men and postmenopausal women (9), and estrogen-replacement therapy substantially reduces the risk of cardiovascular disease in postmenopausal women (22). Although estrogen had little effect on blood pressure in normotensive postmenopausal women (24), it reduced 24-h systolic and diastolic blood pressure (15) and blood pressure response to exercise (21) in postmenopausal women with mild hypertension. Similar findings have been obtained in animal studies. Chronic estrogen treatment lowered blood pressure in some genetic and nongenetic models of hypertension in rats (5, 10). The mechanisms of the cardiovascular benefits of estrogen are not fully understood. The effects of estrogen on lipid and lipoprotein metabolism, glucose metabolism, and hemostasis as well as its direct cardiac and vascular effects are considered as possible explanations (22).
There is evidence to suggest that estrogen may affect cardiovascular function via the autonomic nervous system. Estrogen receptors have been identified in brain centers involved in cardiovascular regulation, e.g., preoptic area, paraventricular nuclei, supraoptic nuclei, nucleus tractus solitarius, ventrolateral medulla, and area postrema (20, 28). Recently, Akaishi and Homma (2) reported that chronic treatment with estrogen blocked the responses of neurons in the periventricular part of the anteroventral third ventricle region to hypertonic saline and ANG II in brain slice preparations obtained from ovariectomized rats. Moreover, the responses of supraoptic vasopressin neurons to changes in blood pressure induced by intravenous injection of phenylephrine or nitroprusside were modified by estrogen in vivo in ovariectomized rats (1). These functional studies suggest that estrogen may be involved in salt and water as well as cardiovascular homeostasis via actions on the central nervous system. The present study was therefore undertaken to examine the effects of estrogen on sympathetic outflow at basal and acutely elevated blood pressure by direct recording of renal and splanchnic nerve activity in conscious unrestrained 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. Female Sprague-Dawley rats (11-16 wk old) 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). All the rats were ovariectomized under ether anesthesia 11 days before the experiment. Ten days after ovariectomy, the rats were anesthetized with methohexital (Brevital, 60 mg/kg ip). Both femoral veins were catheterized with PE-10 tubing. Anesthesia was maintained by supplemental methohexital given intravenously as needed. The right femoral artery was catheterized with PE-50 tubing. Via a left flank incision, the left splanchnic nerve and renal nerve were exposed. A 2- to 3-mm length of each nerve was isolated from the connective tissue and placed on two bipolar silver wire electrodes sutured to the surrounding tissue. When an optimal recording was obtained, the nerves were fixed on the electrodes with silicone rubber (Wacker SilGel 604), and the incisions were closed. The electrode cables and the vascular catheters were tunneled subcutaneously to the back, where they exited. After surgery, the rat was allowed to wake up from anesthesia within 30 min and put in a cage (20 × 22 × 18 cm; width × depth × height), in which it could move freely. The catheters and cables were protected by a spring. Food, tap water, and 20 ml of 5% dextrose were provided.
The experiment was carried out in the same cage 24 h after surgery while the rat was conscious and unrestrained. Food and water were removed during the experiment. The splanchnic nerve and renal nerve signals were amplified by two Gould Universal Amplifiers, with band-pass filters (low 100 Hz, high 1,000 Hz). The raw nerve signals and the signal integrated over 1-s intervals were recorded along with mean and phasic arterial blood pressure and heart rate on a MacLab data acquisition system at a sampling rate of 2,000/s. Nonbiological noise, obtained by recording from the nerves after death, was subtracted from the nerve signals recorded during the experiment. On the day of the experiment, if the ratio of bursting activity to noise for either the renal nerve or splanchnic nerve was
2, the
recording was considered unsatisfactory and data from that nerve were
not used. If the recordings from both the renal and splanchnic nerves
were unsatisfactory, the animal was not used. Less than 20% of the
prepared rats were not used because of unsatisfactory nerve recordings.
The average signal-to-noise ratios were 4.76 ± 2.17 (SD) for the
renal nerve (n = 23) and 5.48 ± 1.85 for the splanchnic nerve (n = 34). A typical recording is presented in Fig.
1.
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Experimental protocols.
In one series of experiments, we determined the effects of the acute
intravenous administration of 17-estradiol
(E2) on renal nerve activity
(RNA), splanchnic nerve activity (SNA), mean arterial blood pressure
(MABP), and heart rate (HR) and the responses to an increase in MABP
with phenylephrine (PE). E2 (150 µg/kg, n = 9) or vehicle
(75 µl/kg, n = 7) was given over a
period of 4 min. The E2 was
dissolved in 100% ethanol and then diluted with an equal volume of
0.9% NaCl to a final concentration of 2 µg/µl. This dose of
E2 can change neuronal activity in
the preoptic and arcuate nuclei of the hypothalamus within 10-20
min (31, 34). PE, dissolved in 0.9% NaCl, was infused intravenously
(6.2 µg · min1 · kg1;
6.2 µl/min) for 30 min beginning 90 min after the injection of
E2.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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There were no differences in basal MABP and HR among the four groups of ovariectomized rats, regardless of whether they were treated with E2 or its vehicle, acutely or chronically (Table 1).
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In the ovariectomized rats in which we examined the effects of acute administration of E2, intravenous injection of E2 resulted in gradual reductions in HR, RNA, and SNA within 20 min to levels that remained lower than those in vehicle-injected rats (Fig. 2). By 90 min after E2 administration, HR had fallen 26 ± 5 beats/min (P < 0.01), and RNA and SNA had fallen 29 ± 6% (P < 0.01) and 25 ± 2% (P < 0.01), respectively. MABP, however, was not affected by the acute injection of E2 and was not different from MABP in the rats given vehicle (Fig. 2). Intravenous injection of vehicle was without significant effect on any of the measured variables.
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Intravenous infusion of PE, beginning 90 min after the injection of E2, caused an increase in MABP and decreases in HR, RNA, and SNA that were not significantly different from those in vehicle-treated rats infused with PE (Fig. 3A). The ratios of changes in HR, RNA, or SNA to changes in MABP, which can be taken as an index of baroreflex gain, were also unaffected by the acute administration of E2 (Fig. 4A).
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The situation, however, in rats chronically treated with E2 was different. The increase in MABP in response to the infusion of PE was smaller in E2-treated than in vehicle-treated rats (P < 0.01), but reductions in HR, RNA, and SNA were similar in both groups (Fig. 3B). The ratios of changes in HR, RNA, and SNA to changes in MABP during the infusion of PE (Fig. 4B) were also higher in the rats chronically treated with E2, but these differences were statistically significant (P < 0.01) only for HR and SNA. The finding that the smaller increase in MABP in response to PE in the rats chronically treated with E2 did not diminish reductions in HR, RNA, and SNA that were similar to those in the vehicle-treated rats suggests that chronic treatment with E2 increased baroreflex sensitivity.
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The present study demonstrates that E2 can inhibit sympathetic outflow in the ovariectomized rat. It is likely that this response is due to an action of E2 on the central nervous system, and, indeed, E2 receptors have been demonstrated in centers in the brain involved in cardiovascular regulation (20, 28). The rapidity of the response, within 20 min, suggests that it may be nongenomic. There is considerable evidence to indicate that sex steroids can bind to cell membranes and induce rapid cellular events within seconds or minutes after application (14, 23). That these rapid effects can occur in the central nervous system is indicated by reports that E2 can inhibit neuronal activity in the preoptic and arcuate nuclei of the hypothalamus within 10-20 min and that this effect was sustained for up to 150 min (31, 34).
Because sympathetic nerves have a tonic effect on vascular tone, a reduction in peripheral resistance is expected when sympathetic nerve activity is decreased. In the present experiments, however, the reductions induced in RNA and SNA by the acute injection of E2 were not accompanied by a change in MABP. It is possible that the E2 increased cardiac output in these experiments, counterbalancing the effect on MABP of the reduced peripheral resistance. This possibility is supported by reports that, in ewes, acute treatment with E2 increased cardiac output while decreasing peripheral resistance (12, 17, 25).
Administration of estrogen attenuates the pressor responses to several vasoconstrictors, such as vasopressin (29), ANG II (17, 25, 35), and adrenergic stimuli (17, 27, 32), in various animal species. In confirmation of this previous work, we have shown that, in the present study, chronic treatment with E2 attenuates the pressor response to intravenous infusion of PE in the ovariectomized rat. The mechanism of this effect of estrogen has not been fully identified. There are a number of reports that estrogen can act directly on the blood vessel to modify responses to vasoactive agents. The nature of this effect is, however, controversial, with some reports that E2 enhances the vasoconstrictor response to catecholamines (3, 4, 30) and others that this response is attenuated by E2 (16, 19, 27). The vascular actions of E2 may be mediated by endothelial factors, such as nitric oxide or modulation of vascular smooth muscle calcium channels (16, 19, 27). Regardless of possible direct effects of E2 on the vasculature in the present study, our findings suggest that chronic treatment with E2 may attenuate the pressor response to PE, at least in part, by increasing baroreflex sensitivity. This is indicated by our observation that, during the infusion of PE, the ratios of reductions in HR and SNA to increases in MABP were greater in E2-treated than in vehicle-treated rats. Consistent with this view are the demonstrations that there are estrogen receptors in the nucleus tractus solitarius (28) and an integrating center for the baroreflex and that E2 can modulate the baroreceptor-induced response of neurons in the supraoptic nuclei (1).
Although E2 has a rapid inhibitory effect on sympathetic activity, a significant attenuation of the pressor response to PE was not seen within 90-120 min after injection of E2. Similarly, Shan et al. (27) reported that the pressor response to norepinephrine was not altered by E2 until 4 h after its injection intravenously. This delayed response suggests that it may be due to a genomic action of E2.
A limitation of the methods currently available for evaluating sympathetic nerve activity is that only changes in nerve activity, rather than absolute activity, can be measured. One must consider, then, the possibility that differences in baseline RNA and SNA in the E2-treated rats, compared with vehicle-treated rats, may have contributed to differences in the responses to the infusion of PE. We believe that this is unlikely. In the rats chronically treated with E2, the ratio of changes in HR and SNA to changes in MABP were both increased during PE infusion compared with the vehicle-treated rats. There was, however, no difference in baseline values for HR. On other hand, in rats acutely treated with E2, the ratios of changes in HR, RNA, and SNA to changes in MABP during the infusion of PE were similar to those in the vehicle-treated rats, even though HR, RNA, and SNA were lower in the E2-treated rats before the start of the PE infusion.
The present experiments have demonstrated that E2 rapidly inhibits sympathetic outflow. This inhibitory effect may persist during the chronic administration of estrogen, since, in women chronically treated with estrogen, circulating levels of norepinephrine and HR are low (11). The withdrawal of sympathetic outflow not only reduces vasomotor tone but also decreases trophic effects on vascular and cardiac muscle (13). This effect may also contribute to the attenuation of the pressor response to vasoconstrictor stimuli and the protection of cardiovascular system by estrogen.
Perspectives
The importance of the sympathetic nervous system in blood pressure regulation is well established. Baroreflex-modulated sympathetic activity is a major factor in the moment-to-moment maintenance of blood pressure. On the other hand, the long-term regulation of blood pressure may be contributed to by hormonal modulation of sympathetic activity (18). It has been shown that a group of hormones, e.g., vasopressin, ANG II, atrial natriuretic peptide, and endothelin, can modulate sympathetic activity via direct effects on the central nervous system (8, 18). The present report is the first to demonstrate that E2 can inhibit sympathetic outflow. This effect may be enhanced by signals from the baroreceptors. Under normal circumstances, the inhibition of sympathetic activity is not sufficient to affect arterial blood pressure. When blood pressure is raised, however, an increase in baroreceptor input may enhance the inhibitory effect of estrogen on sympathetic outflow and facilitate the return of blood pressure to relatively normal levels. This hypothesis is supported by observations of ours and others that treatment of experimental animals with E2 has little or no effect on basal arterial blood pressure but markedly attenuates the pressor response to pressor agents (17, 25, 27, 29, 32, 35). Moreover, treatment of postmenopausal women with estrogen does not affect blood pressure in normotensive subjects (24) but reduces blood pressure in hypertensive subjects, with a correlated reduction in circulating norepinephrine (15).The importance of increased RNA in various animal models of hypertension is indicated by the demonstration that the development of the hypertension is delayed and attenuated by renal denervation (7). This suggests that the inhibition of RNA by E2, which we have shown occurs acutely, may, if it is sustained chronically, be particularly significant in the long-term regulation of arterial blood pressure. There is evidence that estrogen may affect both the renin-stimulating and antinatriuretic effects of the renal sympathetic nerves. Plasma renin or renin activity was reduced 25-40% in postmenopausal women treated chronically with estrogen (6, 26). In rats treated with DOC and salt, chronic E2 treatment, which attenuated the hypertension, increased sodium and water intake but decreased body weight (5), suggesting enhanced renal sodium excretion. DOC-salt hypertension is also blunted by renal denervation (7).
In conclusion, estrogen participates in physiological and pathophysiological cardiovascular regulation. It is possible that the cardioprotective action of estrogen involves in part an inhibitory action on the sympathetic nervous system.
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ACKNOWLEDGEMENTS |
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This research was supported by National Heart, Lung, and Blood Institute Grants HL-19209 and HL-12990.
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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: L. Share, Dept. of Physiology and Biophysics, University of Tennessee, Memphis, 894 Union Ave., Memphis, TN 38163.
Received 3 February 1998; accepted in final form 3 June 1998.
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) in HR, RNA, and SNA. RNA and SNA are expressed as percentage of
preinjection values, which were taken as 100%.
* P < 0.05;
** P < 0.01, E2 vs. vehicle.
