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Department of Physiology, College of Medicine, Northeastern Ohio Universities, Rootstown, Ohio 44272
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Arterial
pressure (AP), heart rate (HR), cardiac sympathetic tonus (ST), and
parasympathetic tonus (PT) were determined in spontaneously
hypertensive rats (SHR, 8 male and 8 female) and Wistar-Kyoto
normotensive rats (WKY, 8 male and 12 female) before and after acute
exercise. Before exercise, hypertensive rats (regardless of gender) had
an increased ST (+15 beats/min), increased resting HR (+12 beats/min),
and decreased PT (
11 beats/min). Similarly, female rats
(regardless of strain) also had an increased ST (+15 beats/min),
increased resting HR (+39 beats/min), and decreased PT (14
beats/min). Hypertensive rats had a significant reduction in AP
(17 ± 3 mmHg), ST (26 beats/min), PT (7
beats/min), and HR (14 beats/min) after exercise. In contrast,
AP was not reduced in normotensive rats and ST (+18 beats/min) and HR
(+42 beats/min) were increased in female normotensive rats after
exercise. However, male normotensive rats had a postexercise reduction
in ST (14 beats/min) and HR (19 beats/min). In summary,
AP, ST, and resting HR were higher whereas PT was lower in hypertensive
vs. normotensive rats. Furthermore, females had a higher resting HR,
intrinsic HR, and ST and lower PT than male rats. These data
demonstrate that gender and the resting level of AP influence cardiac
autonomic regulation.
hypertension; blood pressure; heart rate; autonomic nervous system; spontaneously hypertensive rats; Wistar-Kyoto rats
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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GENDER, SEDENTARY LIFESTYLE, AND HYPERTENSION are risk factors associated with cardiovascular diseases (CVD) (13, 20). Available data suggest that increased levels of physical activity and reductions in arterial pressure (AP) reduce cardiovascular risks by their influence on the autonomic nervous system (ANS). Similarly, gender influences the ANS regulation of the cardiovascular system (6, 7). Recent data support the view that estrogen provides a degree of cardiovascular protection from CVD by its influence on the ANS and, more particularly, on cardiac autonomic nerve activity (12).
Recently, several investigators have indirectly determined the influence of the ANS on cardiovascular regulation by determining sympathetic tonus (ST) and parasympathetic tonus (PT) (16, 19, 24). Recent work has demonstrated that ST and PT reflect changes in heart rate (HR) and are an appropriate method for indirectly determining the influence of the ANS on cardiovascular regulation (24).
Our study was designed to determine if the level of resting AP (normotensive vs. hypertensive) and gender (male vs. female) influence postexercise cardiac autonomic responses. Because hypertension, elevated levels of cardiac sympathetic activity, gender, and sedentary lifestyle are significant cardiovascular risk factors, we examined the influence of these factors on postexercise cardiovascular responses.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Design
We tested the hypothesis that the resting level of AP (hypertension vs. normotension) and gender influence postexercise cardiac autonomic responses. Sixteen male [8 spontaneously hypertensive rats (SHR) and 8 Wistar-Kyoto (WKY) rats] and twenty female (8 SHR and 12 WKY) rats were weaned at 4 wk of age and housed in standard rat cages at all times. After 8 wk, rats were chronically instrumented with arterial catheters. After 4-5 days of recovery, four experimental protocols were conducted. Each protocol was randomized and separated by at least 48 h. Protocol 1 determined postexercise mean arterial pressure (MAP) and HR. Protocol 2 determined ST and PT at rest in a no-exercise condition. Protocol 3 determined ST and PT in a postexercise condition. Finally, protocol 4 determined ST during a single bout of dynamic exercise.Surgical Procedures
All instrumentation was performed using aseptic surgical procedures. Anesthesia was obtained with a mixture of ketamine (40 mg/kg), xylazine (8 mg/kg), and chloropromazine (4 mg/kg), and supplemental doses were administered as needed. Rats were instrumented with a polytetrafluoroethylene catheter inserted into the descending aorta via the left common carotid artery for measurements of AP, MAP, and HR. The arterial catheter was also used for the infusion of cardiac autonomic antagonists. The arterial catheter was flushed daily, filled with heparin (1,000 U/ml), and plugged with a paraffin-filled obturator. Rats were carefully monitored for signs of infection and changes in body weight during recovery from the surgery. During this time, the rats were familiarized with the treadmill and experimental procedures during two to four training sessions. The training sessions assured that the experimental procedures would not be novel to the rat and that the rat would run without the use of aversive stimuli. At the time of the experimental protocols, all rats had recovered and were healthy and gaining weight.Experimental Measurements
AP was determined by connecting the arterial catheter to a Gould P23XL pressure transducer coupled to a Gould RS3600 physiograph. MAP was derived electronically with a low-pass filter. HR was determined with a Gould electrocardiograph/biotach model 20-4615-65 that was triggered from the AP pulse. All data were displayed on the physiograph and sampled by a data-acquisition system (MacLab 8 analog-to-digital converter, Analog Digital Instruments) and laboratory computer (Macintosh Performa 5200CD) for subsequent analysis.Experimental Protocols
Protocol 1: Determination of postexercise MAP and HR. The rats were allowed to adapt to the laboratory environment for 1 h so that baseline hemodynamic variables could be obtained. Subsequently, each rat ran on a motor-driven treadmill at 12 m/min and at a 10% grade for 40 min. By using this relatively low workload with no aversive stimuli and providing training sessions, we feel we are truly studying a response to exercise rather than a response to stress. After exercise, each rat was monitored for an additional 60 min.
Protocol 2: Determination of ST and PT; no exercise.
Two trials were required to determine cardiac ST and PT. On
day
1, the rats were placed unrestrained
in a large Plexiglas box (30.5 × 30.5 × 30.5 cm). The rats
were allowed to adapt to the laboratory environment for 1 h so that
baseline hemodynamic variables could be obtained. After the adaptation
period, the HR, AP, and MAP responses to cardiac autonomic sympathetic
and parasympathetic blockade
(
1-adrenergic and
muscarinic-cholinergic receptor blockade) were determined. Drug doses
for the sympathetic and parasympathetic antagonists were calculated
relative to the animal's body weight on each experimental day. Cardiac
muscarinic-cholinergic receptor blockade was achieved by infusion of
the nonspecific muscarinic-cholinergic receptor antagonist scopolamine
methyl nitrate [methscopolamine (MS) 3 mg/kg] through the
carotid arterial catheter. Because the HR response to MS reached its
peak in 10-15 min, this time interval was standardized before the
HR measurement. Cardiac
1-adrenergic receptor blockade
was achieved by infusion of the specific
1-adrenergic receptor
antagonist metoprolol (MT, 10 mg/kg) into the carotid arterial
catheter. MT was infused 15 min after MS, and again the HR response was
measured after 15 min. The entire data collection took ~2 h. At the
end of the experiment, the rats were returned to their housing
facilities. On an alternate day (>48 h),
trial
2 was conducted. Rats were treated
identically as described in trial
1 except that the order of blockade
was reversed. Intrinsic HR (HRi)
was considered to be the HR after complete cardiac autonomic blockade
(muscarinic-cholinergic and 1-adrenergic receptor
blockades). ST was calculated as
HRm HRi and PT as
HR
HRi, where
HRm is HR after
muscarinic-cholinergic receptor blockade and
HR is HR after
1-adrenergic receptor blockade.
Protocol 3: Determination of ST and PT; postexercise.
Experimental trials
1 and
2 were repeated after a single bout of
dynamic exercise. The procedures were identical as described above
except that the adaptation time was replaced by a single bout of
treadmill running. Each rat ran on a motor-driven treadmill at 12 m/min
at a 10% grade for 40 min. Twenty minutes after exercise, cardiac
autonomic blockade was performed as described above.
1-adrenergic and
muscarinic-cholinergic receptor-blocking agents were administered 20 min after exercise to study autonomic tonus at a time when postexertional hypotension (PEH) is present as demonstrated in protocol
1. All measures of autonomic tonus, as
described for the no-exercise protocol, were made during this
steady-state period. These postexercise measures of autonomic tonus are
highly reliable as demonstrated by similar results reported in two
previous studies from this laboratory (5, 6). The order of drug
administration was randomized for both the no-exercise and postexercise
protocols. The effectiveness of the muscarinic-cholinergic and
1-adrenergic receptor blockade
(determined at the completion of
protocols
2 and
3) was evaluated by the change in HR
in response to changes in AP produced by intra-arterial infusion of
phenylephrine hydrochloride (1.5 µg/kg) and nitroglycerin (0.15 mg/kg).
Protocol 4: Determination of ST during exercise.
Cardiac ST was determined during a single bout of dynamic treadmill
exercise. On the day of the experiment, each rat was placed on the
treadmill and allowed to adapt to the laboratory environment for 1 h so
that baseline hemodynamic variables could be obtained. Subsequently,
each rat ran on a motor-driven treadmill at 12 m/min at a 10% grade
for 10 min or until HR, AP, and MAP had reached a steady state. Once
steady state was achieved, muscarinic-cholinergic receptor blockade was
achieved by infusion of the nonspecific muscarinic cholinergic receptor
antagonist MS (3 mg/kg) through the carotid arterial catheter. The
animal continued to run for an additional 10-15 min or until HR,
AP, and MAP had again reached a new steady-state level. Subsequently,
cardiac 1-adrenergic receptor
blockade was achieved by infusion of the specific
1-adrenergic receptor
antagonist MT (10 mg/kg) into the carotid arterial catheter. Each rat
ran for an additional 10-15 min to allow for complete expression of
1-adrenergic receptor blockade.
Once new steady-state HR, AP, and MAP were established, the treadmill
was stopped and the test was terminated.
Drugs
MS and MT were purchased from Sigma (St. Louis, MO). Phenylephrine hydrochloride was purchased from Winthrop-Breon (New York, NY). Nitroglycerin was purchased from LyphoMed (Chicago, IL). Ketamine hydrochloride was purchased from Aldrich Chemical (Milwaukee, WI). Chloropromazine hydrochloride was purchased from Rugby Laboratories, and xylazine was purchased from Mobay.Data Analysis
All data are expressed as means ± SE. A two-way analysis of variance (ANOVA) was used to compare age, body weight, HRi and resting HR, and MAP between groups (Table 1). In all four groups of rats, t-tests were used to compare differences between body weights on the day of surgery and experimental days. A two-way ANOVA with repeated measures was used for each of the following comparisons: 1) MAP before, during, and after exercise between male SHR and WKY rats (Fig. 1A) and female SHR and WKY rats (Fig. 1C); and 2) HR before, during, and after exercise between male SHR and WKY rats (Fig. 1B) and female SHR and WKY rats (Fig. 1D). Differences observed over time were further evaluated using a test of simple effects post hoc analysis. A three-way ANOVA (strain × gender × exercise) with repeated measures on the third factor was used to compare ST (Fig. 2) and PT (Fig. 3). Significant interactions for both of these variables allowed for further intergroup comparisons to be made using a test of simple effects post hoc analysis. ST, PT, and cardiac autonomic balance (CAB) were correlated with HR. CAB was calculated as ST + PT. A regression analysis was used to determine the relationship between 1) ST vs. HR, 2) PT vs. HR, and 3) CAB vs. HR (Fig. 4) during the no-exercise, exercise, and postexercise protocols. An alpha level of 0.05 was used to determine statistical significance.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The effectiveness of muscarinic-cholinergic and
1-adrenergic receptor blockade
was evaluated by the change in HR in response to changes in AP produced
by infusions of phenylephrine and nitroglycerin. After blockade in the
SHR, phenylephrine produced a 30 ± 3 mmHg increase in MAP with a
decrease in HR of 3 ± 1 beats/min. Nitroglycerin produced a 38 ± 4 mmHg decrease in MAP, with an increase in HR of 2 ± 1 beats/min. Similarly, in the WKY rats, phenylephrine produced a 29 ± 6 mmHg increase in MAP, with a decrease in HR of 2 ± 1 beats/min. Nitroglycerin produced a 29 ± 2 mmHg decrease in MAP
with an increase in HR of 3 ± 1 beats/min.
Table 1 presents age, body weight on the day of surgery and on the experimental days, intrinsic and resting HR, and resting MAP from the no-exercise protocols for the four groups of rats. Although the ages of the rats were not different between groups, male rats were significantly heavier than female rats. Body weights on the experimental days were not significantly different from body weights on the day of surgery, with the exception of the female WKY rats. Female WKY rats were significantly heavier on experimental days than on their day of surgery. Both gender and strain influenced resting HR, whereas only strain influenced resting AP. As expected, resting AP and HR were higher in SHR vs. WKY rats. Females (regardless of strain) had higher resting HR and HRi than males.
Protocol 1: Determination of postexercise MAP and HR. Ten minutes after exercise, MAP significantly decreased 16 ± 5 mmHg in male SHR (Fig. 1A). This PEH persisted for the duration of the postexercise period. In contrast, MAP was not reduced in the male WKY rats (Fig. 1A). Twenty minutes after exercise, MAP significantly decreased 17 ± 4 mmHg in female SHR (Fig. 1C). This PEH persisted for the duration of the postexercise period. MAP was not reduced in the female WKY rats (Fig. 1C).
Thirty minutes after exercise, HR significantly decreased in both male SHR and WKY rats (10 ± 3 beats/min and 19 ± 3 beats/min respectively, Fig. 1B). This bradycardia persisted for the duration of the postexercise period. Forty minutes after exercise, HR significantly decreased (17 ± 4 beats/min, Fig. 1D) in female SHR. This bradycardia persisted for the duration of the postexercise period. In contrast, HR remained significantly above the preexercise control (42 ± 6 beats/min, Fig. 1D) in female WKY rats. This tachycardia persisted for the entire postexercise period. HR and MAP responses to cardiac autonomic sympathetic and parasympathetic blockade (muscarinic-cholinergic and1-adrenergic receptor blockade)
were determined in protocols
2-4.
Cardiac autonomic blockade did not significantly change MAP in any of
these conditions. This is an important consideration because changes in
pressure would have reflexly altered HR.
Protocols 2 and 3: ST in the no-exercise and postexercise condition. Figure 2 presents ST in male SHR and WKY rats (A) and female SHR and WKY rats (B) in the no-exercise and postexercise conditions. Both strain and gender influenced no-exercise ST. Specifically, in the no-exercise condition, ST was significantly greater in SHR (34%) vs. WKY rats. Similarly, ST was significantly greater in female (SHR 65 ± 1 and WKY 46 ± 2 beats/min) vs. male (SHR 45 ± 2 and WKY 35 ± 2 beats/min) rats.
Both strain and gender also influenced postexercise ST. A single bout of dynamic exercise decreased ST in male SHR (43%), male WKY (40%) and female SHR (48%) (Fig. 2, A and B). In contrast, postexercise ST was significantly increased in the female WKY rats (39%) (Fig. 2B). Acute exercise normalized ST in male SHR (postexercise, male SHR 26 ± 2 beats/min, male WKY 21 ± 2 beats/min). In contrast, postexercise ST was not normalized in female (34 ± 2 beats/min) relative to male (26 ± 2 beats/min) SHR. In contrast, postexercise ST was lower in female SHR (34 ± 2 beats/min) vs. female WKY (64 ± 5 beats/min) rats.Protocols 2 and 3: PT in the no-exercise and postexercise condition.
Figure 3 presents PT in male SHR and WKY rats
(A) and female SHR and WKY rats
(B) in the no-exercise and
postexercise conditions. Both strain and gender influenced no-exercise
PT. In the no-exercise condition, PT was significantly lower in SHR
(38%) vs. WKY rats. This difference was primarily due to the lower PT
in female SHR compared with female WKY rats (3 ± 2 vs.
23 ± 3 beats/min). PT was also significantly lower in female
(SHR 3 ± 2 and WKY 23 ± 3 beats/min) vs. male
(SHR 28 ± 1 and WKY 26 ± 2 beats/min) rats.
However, this difference was again primarily due to the lower PT in
female SHR because there was no significant difference between male and
female WKY rats (26 ± 2 vs. 23 ± 2 beats/min).
1 ± 2 and WKY 4 ± 1 beats/min) compared with male (SHR 16 ± 2 and WKY 10 ± 3 beats/min) rats in the postexercise condition.
Protocol 4: Relationship between ST, PT, and CAB and HR. ST during exercise was 110 ± 3, 106 ± 2, 117 ± 7, and 142 ± 5 beats/min in SHR males and females and WKY males and females, respectively. CAB was calculated during both the no-exercise and postexercise protocols. CAB during the no-exercise and postexercise protocols, respectively, was as follows: male SHR, 17 ± 2 and 10 ± 3 beats/min; female SHR, 62 ± 2 and 32 ± 4 beats/min; male WKY, 9 ± 3 and 11 ± 4 beats/min; and female WKY, 22 ± 3 and 61 ± 5 beats/min. Figure 4 presents the relationship between HR and ST (A), PT (B), and CAB (C) during the no-exercise, exercise, and postexercise protocols for all four groups of rats. ST and CAB are highly predictive of HR, as demonstrated by strong positive correlations between ST vs. HR (r = 0.973, P = 0.0001) and CAB vs. HR (r = 0.894, P = 0.003).
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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AP, ST, and resting HR were higher whereas PT was lower in hypertensive vs. normotensive rats. Furthermore, gender influenced HR and cardiac autonomic tonus. Specifically, females had a higher resting HR, HRi, and ST and lower PT than male rats. Taken together, these data demonstrate that gender and the resting level of AP influence cardiac autonomic regulation.
A single bout of dynamic exercise also altered cardiac autonomic regulation. Specifically, acute exercise reduced postexercise AP, HR, ST, and PT in hypertensive rats. The postexercise reduction in ST was larger whereas the reduction in PT was smaller in female hypertensive rats. In contrast, acute exercise did not reduce postexercise AP in normotensive rats. Furthermore, although postexercise ST and HR were reduced in male normotensive rats, postexercise ST and HR were increased in female normotensive rats. These data demonstrate that gender and the resting level of AP also influence postexercise cardiac autonomic regulation.
Influence of Resting AP (Normotensive vs. Hypertensive)
Elevations in sympathetic nerve activity are associated with the development and maintenance of hypertension (21, 22, 28). Thus our findings of an elevated ST and HR and reduced PT in hypertensive rats are consistent with previous results (18, 22, 23). The reduction in AP and HR in hypertensive rats after exercise was associated with a decreased ST. Similarly, a postexercise reduction in AP was associated with a decreased ST (5, 6), decreased directly measured peripheral SNA (15), and decreased renal and mesenteric SNA (27, 31) in hypertensive rats and humans (5, 6, 15, 27, 31). These data suggest that acute exercise may be associated with a general sympathoinhibition in hypertensive subjects.In contrast, acute exercise did not reduce postexercise AP in normotensive rats. These data suggest that differential mechanisms are controlling postexercise hemodynamics in hypertensive and normotensive rats. Specifically, sympathoinhibition, bradycardia, and hypotension occurred after exercise in hypertensive rats. In contrast, female WKY rats demonstrated a sympathoexcitation and tachycardia without a reduction in AP. Although male normotensive rats had postexercise bradycardia and decreased ST, AP was not reduced.
Influence of Gender on No-Exercise Cardiac Autonomic Tonus
Female hypertensive and normotensive rats had a higher ST, HR, and HRi and lower PT than their male counterparts (Fig. 2 and Table 1). The higher ST and lower PT in female rats is consistent with the higher resting HR compared with the male rats. These results are consistent with reports of elevated resting HR in both normotensive (1, 4) and hypertensive females (3, 4, 6, 14).Contrary to the influence that gender exerts on resting HR, there was no influence of gender on resting MAP, regardless of strain (hypertensive vs. normotensive). Similar results have been reported for normotensive (7) and hypertensive (3) male and female rats. In contrast, a previous study from this laboratory reported a gender influence on resting MAP, in that female SHR had lower blood pressures than male SHR (6). Calhoun et al. (4) also reported that baseline MAP was greater in male than female SHR. The reasons for the differences between studies are unknown. Thus there is no clear consensus on the influence of gender on resting MAP.
We were surprised to find that female rats had a higher ST and lower PT than male rats because increased sympathetic and decreased parasympathetic activity are associated with an enhanced risk for cardiac arrhythmias and sudden cardiac death (SCD) (26, 30). However, the incidence of arrhythmias and SCD in females is lower than in males (8, 13). This apparent paradox merits further investigation.
Influence of Gender on Postexercise Cardiac Autonomic Tonus
Female normotensive rats had an increased postexercise ST and HR without a corresponding PEH. In contrast, male normotensive rats had a decreased postexercise ST and HR also without a corresponding PEH. It is possible that the increased ST is reflective of a general sympathoexcitation and that a postexercise reduction in AP was prevented in female normotensive rats because of the postexercise sympathoexcitation. However, PEH may have been prevented in the male normotensive rats by another mechanism. Specifically, male normotensive rats have an increased vasoconstrictor response to catecholamines compared with female normotensive rats (29). These data suggest that a lower level of SNA in males may be sufficient to maintain AP. Thus females may maintain postexercise AP by increasing SNA whereas males may rely on an increased vascular response to catecholamines.A single bout of exercise reduced PT in both normotensive and hypertensive male and female rats. These results are consistent with previous investigations that documented a reduction in the parasympathetic influence on HR after a single bout of exercise in normotensive men and women (2, 25) and hypertensive male and female rats (6). Thus, unlike ST, which had a differential response between male and female normotensive rats, the postexercise reduction in PT was consistent between genders.
ST, PT, and CAB as Measures of Cardiac Autonomic Function
ST and CAB were significantly associated with HR at rest, during exercise, and after exercise (Fig. 4). Although PT did not correlate significantly with HR, when the two branches of the ANS are combined (CAB), they are strongly predictive of HR. This was expected because in hypertensive rats, parasympathetic activation of sinus node activity is overwhelmed by the dominance of sympathetic activity (6). Thus ST, PT, and CAB are an indication of HR and may be used as an indirect indicator of cardiac autonomic nerve activity (5, 6, 16, 24). Furthermore, experimental results assessed by measures of ST are consistent with results obtained using direct measures of nerve activity. For example, postexercise reductions in cardiac ST (5, 6) are consistent with postexercise reductions in directly measured muscle SNA (15). Similarly, exercise training-induced reductions in cardiac ST (6) are consistent with exercise training-induced reductions in directly measured renal (10, 24) and muscle SNA (17). Finally, exercise-induced elevations in directly measured SNA (9, 11) are consistent with exercise-induced increased ST. Thus alterations in cardiac autonomic tonus may directly reflect changes in cardiac autonomic nerve activity.Limitations
It is important to note that male normotensive rats showed a decreased postexercise ST and HR with no reduction in MAP. Furthermore, female normotensive rats had an elevated postexercise ST and HR with no corresponding increase in MAP. These observations appear to dissociate a link between cardiac ST and AP. Thus measures of cardiac autonomic activity may not accurately reflect AP.It is also important to remember that measurements of autonomic tonus are indirect assessments of nerve activity and therefore may be influenced by changes in receptor number, receptor agonist affinity, and/or alterations in second-messenger signaling. Furthermore, measures of tonus were determined from sequential blockade of the two limbs of the ANS. It is possible therefore that blockade of one limb of the ANS altered the tone of the remaining limb through some as yet undetermined mechanism. For example, if administration of one antagonist altered contractility, cardiopulmonary or arterial baroreflex function, or other CNS-mediated responses, it is possible that the tone in the remaining limb will be affected. It is unknown, however, what if any effect activation of these other mechanisms would have on our measurements. Thus it may be important to keep these concerns in mind when evaluating the data.
In summary, AP, resting HR, and ST were higher whereas PT was lower in hypertensive vs. normotensive rats. Similarly, female rats had higher resting HR and HRi and ST and lower PT than male rats. After a single bout of dynamic exercise, hypertensive rats had a significant reduction in MAP and HR that was accompanied by a reduced ST and PT. In contrast, MAP was not reduced after exercise in normotensive rats. Furthermore, although ST and HR were increased in female normotensive rats after exercise, male normotensive rats had a postexercise reduction in ST and HR. These results demonstrate that gender and resting AP influence cardiac autonomic regulation in a no-exercise and postexercise condition.
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ACKNOWLEDGEMENTS |
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We thank David W. Rodenbaugh for skillful technical assistance.
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FOOTNOTES |
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This work was supported by the National Heart, Lung, and Blood Institute Grant HL-45245 and by the American Heart Association, Ohio Affiliate, Grant AK-95-02-S.
Address for reprint requests: S. E. DiCarlo, Dept. of Physiology, College of Medicine, Northeastern Ohio Universities, 4209 State Route 44, PO Box 95, Rootstown, OH 44272.
Received 23 April 1997; accepted in final form 31 October 1997.
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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) and Wistar-Kyoto (WKY, 
) rats. MAP was significantly
decreased by 10 min (male SHR 16 ± 5 mmHg,
A) and 20 min (female SHR 17 ± 4 mmHg, C) postexercise and continued
to be so for the duration of the 60-min postexercise period. There was
a significant bradycardia in male and female SHR and male WKY rats
during the postexercise period. However, there was a significant
tachycardia in the female WKY rats during the entire postexercise
period. bpm, Beats/min. * P < 0.05 preexercise vs. postexercise;
P < 0.05 SHR vs. WKY.
P < 0.05 male vs. female.
