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Am J Physiol Regul Integr Comp Physiol 281: R375-R380, 2001;
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Vol. 281, Issue 2, R375-R380, August 2001

Central blockade of vasopressin V1 receptors attenuates postexercise hypotension

Heidi L. Collins, David W. Rodenbaugh, and Stephen E. DiCarlo

Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

We tested the hypothesis that central arginine vasopressin (AVP) mediates postexercise reductions in arterial pressure (AP) and heart rate (HR). To test this hypothesis, nine spontaneously hypertensive rats (SHR) were instrumented with a 22-gauge stainless steel guide cannula in the right lateral cerebral ventricle and with a carotid arterial catheter. After the rats recovered, AP and HR were assessed before and after a single bout of dynamic exercise with the central administration of vehicle or the selective AVP V1-receptor antagonist d(CH3)5 Tyr(Me)-AVP (AVP-X). AP and HR were significantly decreased below preexercise values with central administration of vehicle [P < 0.05, change (Delta )-21 ± 4 mmHg and Delta -20 ± 6 beats/min, respectively]. In sharp contrast, after exercise with central administration of AVP-X, both AP (Delta +8 ± 5 mmHg) and HR (Delta +24 ± 9 beats/min) were not significantly different from preexercise values (P > 0.05). Furthermore, AVP-X at rest did not significantly alter AP (181 ± 11 vs. 178 ± 11 mmHg, P > 0.05) or HR (328 ± 24 vs. 331 ± 22 beats/min, P > 0.05). Thus central blockade of AVP V1 receptors prevented postexercise reductions in AP and HR. These data suggest that AVP, acting within the central nervous system, mediates postexercise reductions in AP and HR in the SHR.

arginine vasopressin; arterial baroreflex resetting; cardiopulmonary baroreflex


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

HEART DISEASE IS THE LEADING cause of death in the United States, and hypertension is a leading risk factor for heart disease. Thus interventions designed to reduce arterial pressure (AP) remain the focus of numerous investigative efforts. A single bout of dynamic exercise reduces postexercise AP for several hours in hypertensive individuals and animals (16, 28). Understanding the mechanisms responsible for the postexercise reduction in AP may lead to measures designed to lower AP in hypertensive individuals. The postexercise hypotension (PEH) requires intact cardiopulmonary (11) and arterial baroreceptors (8). Furthermore, PEH is mediated by a resetting of the operating point of the arterial baroreflex to a lower pressure (9, 21). Arterial baroreflex resetting can occur by facilitation of cardiopulmonary reflexes (5).

Arginine vasopressin (AVP), acting primarily on V1 receptors, enhances both cardiopulmonary (1, 25, 42) and arterial baroreflex function (4, 17, 42) as well as resets the operating point of the arterial baroreflex to a lower pressure (23). Furthermore, Stebbins and colleagues (6, 38) have demonstrated that AVP acts at the area postrema to enhance arterial baroreflex-induced sympathoinhibition during static muscle contraction. Sympathoinhibition also contributes, in part, to PEH (20, 21, 29). Finally, AVP is increased in dorsal brain stem areas during dynamic exercise (32). Taken together, these data support a possible mechanism whereby an AVP-induced facilitation of inhibitory cardiopulmonary reflexes and/or resetting of the operating point of the arterial baroreflex may contribute to PEH. Therefore, this study was designed to test the hypothesis that central administration of a selective AVP V1-receptor antagonist would attenuate postexercise reductions in AP in spontaneously hypertensive rats (SHR).


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Design. Nine male SHR were weaned at 4 wk of age and housed in standard rat cages at all times. Between 12 and 13 wk of age, all rats were instrumented with a stainless steel guide cannula in the lateral cerebral ventricle. After ~2 wk of recovery, all rats were instrumented with a carotid arterial catheter and were subsequently allowed at least 5 days to recover. After the rats recovered, AP and heart rate (HR) were recorded before and after a single bout of dynamic exercise with the central administration of vehicle or the selective AVP V1-receptor antagonist d(CH3)5Tyr(Me)-AVP (AVP-X). In addition, all rats underwent a sham-exercise protocol that served as a time control. All surgical and experimental procedures were approved by the Institutional Animal Care and Use Committee and were conducted in conformity with the Guide for the Care and Use of Laboratory Animals.

Surgical procedures. All instrumentation was performed using aseptic surgical procedures. Rats were anesthetized with an intramuscular injection of ketamine hydrochloride (40 mg/kg), xylazine (8 mg/kg), and chlorpromazine hydrochloride (4 mg/kg). Subsequently, each rat was placed into a cranial stereotaxic instrument (Kopf, Tujunga, CA), and a 22-gauge stainless steel guide cannula (Plastics One, Roanoke, VA) was inserted into the right lateral cerebral ventricle (coordinates to bregma: 1.5 mm lateral, 1 mm posterior, and 3.2 mm ventral to the skull) (27) and affixed with cranioplastic cement. A dummy cannula was placed into the guide cannula to maintain patency. After a 2-wk recovery period, all rats were instrumented with a polytetrafluoroethylene catheter inserted into the descending aorta via the left common carotid artery for measurements of AP, mean AP (MAP), and HR (8, 9, 11, 29). The arterial catheter was flushed daily with heparinized saline, filled with heparin (1,000 U/ml), and plugged with a stainless steel obturator. The animals were allowed at least 5 days to recover. Rats were carefully monitored for signs of infection and changes in body weight during the recovery period. During this time, the rats were familiarized with the treadmill and experimental procedures. The training sessions assured that the experimental procedures would not be novel to the rat and that the rat would run without any aversive stimuli. At the time of the experimental protocol, all rats were healthy and gaining weight.

Experimental measurements. AP and HR were 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) and laboratory computer (Macintosh Performa 5200CD) for subsequent analysis.

Experimental protocols. On the day of the experiment, the rats were allowed to adapt to the laboratory environment for 60 min so that baseline hemodynamic variables could be obtained. After the adaptation period, each rat ran on a motor-driven treadmill at 12 m/min, 10% grade for 40 min. By using this relatively low workload with no aversive stimuli and providing training sessions, we feel that we are truly studying a response to exercise rather than a response to stress. Immediately after exercise, each rat received an intracerebroventricular injection of vehicle (10 µl saline over 30 s) and was monitored for 60 min. The entire data collection took ~3.5 h. At the end of the experiment, the rats were returned to their housing facilities. On an alternate day (>48 h), these procedures were repeated except that the rats received an intracerebroventricular injection of AVP-X (100 ng in 10 µl). This dose was selected because several studies (7, 15, 27, 35) have used similar doses or equipotent doses of other AVP V1-receptor antagonists (31) and reported reductions in the pressor response to centrally applied AVP but not to the pressor response to intravenous AVP. Furthermore, this dose has minimal agonist-like properties (15). The order of central AVP-X or vehicle was alternated between animals. All rats also underwent a sham-exercise protocol that served as a time control. During this protocol, AP and HR were recorded during a 60-min control period, following 40 min of sitting on the treadmill (sham exercise), and for a 60-min "recovery" period.

The effect of an intracerebroventricular injection of AVP-X on resting hemodynamic variables was determined in five rats. Control values for AP and HR were recorded over a 30-min period. Subsequently, each rat received an intracerebroventricular injection of AVP-X (100 ng in 10 µl), and AP and HR were continuously recorded for 20 min.

Evaluation of pre- and postexercise hemodynamics. Beat-to-beat AP and HR were continuously recorded throughout the experimental protocols. After the adaptation period, beat-to-beat AP and HR were averaged for a 30-min period to obtain the preexercise value. Beat-to-beat AP and HR were averaged over the 60-min postexercise period to obtain the postexercise value. The pre- and postexercise averages were compared to determine the influence of central AVP-X on postexercise hemodynamic responses.

Data analysis. All data are expressed as means ± SE. Student's paired t-tests were used to compare MAP and HR for each experimental protocol of 1) before and after exercise under each experimental condition (vehicle and AVP-X) and 2) before and after AVP-X at rest. An alpha level of 0.05 was used to determine statistical significance.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

After exercise with central administration of vehicle, MAP was significantly below the preexercise level [P < 0.05, change (Delta )-21 ± 4 mmHg; Fig. 1A]. In sharp contrast, after exercise with central administration of AVP-X, MAP was not significantly different from the preexercise level (P > 0.05, Delta +8 ± 5 mmHg; Fig. 1B). Finally, a 40-min session of sham exercise (resting on the treadmill) did not significantly alter AP (P > 0.05, Delta +4 ± 5 mmHg; Fig. 1C). Similarly, after exercise with central administration of vehicle, HR was significantly below the preexercise level (P < 0.05, Delta -20 ± 6 beats/min; Fig. 2A). Again, in sharp contrast, after exercise with central administration of AVP-X, HR was not significantly different from the preexercise level (P > 0.05, Delta +24 ± 9 beats/min; Fig. 2B). Finally, sham exercise did not alter HR (P > 0.05, Delta +10 ± 7 beats/min; Fig. 2C).


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  		Fig. 1.   Mean arterial pressure (MAP) before and after exercise with central administration of vehicle (A) or central blockade of vasopressin V1 receptors [d(CH3)5 Tyr(Me)-arginine vasopressin (AVP) (AVP-X); B]. C: MAP before and after a 40-min session of sham exercise (resting on the treadmill). A significant reduction in MAP following exercise [postexercise hypotension (PEH)] was observed with the central administration of vehicle (Delta -21 ± 4 mmHg; A). In sharp contrast, after exercise with central administration of AVP-X, arterial pressure was not different from preexercise values (Delta +8 ± 5 mmHg; B). Finally, a 40-min session of sham exercise did not significantly alter arterial pressure (Delta +4 ± 5 mmHg; C). These data support the conclusion that central vasopressin contributes, in part, to PEH. *P < 0.05.



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  		Fig. 2.   Heart rate (HR) before and after exercise with central administration of vehicle (A) or central blockade of vasopressin V1 receptors (AVP-X; B). C: HR before and after a 40-min session of sham exercise (resting on the treadmill). After exercise with central administration of vehicle, HR was significantly below the preexercise level (Delta -20 ± 6 beats/min; A). With central administration of AVP-X, HR was not significantly different from the preexercise level (Delta +24 ± 9 beats/min; B). Finally, a 40-min session of sham exercise did not alter HR (Delta +10 ± 7 beats/min; C). *P < 0.05.

AVP-X at rest did not significantly alter AP (181 ± 11 vs. 178 ± 11 mmHg, P > 0.05) or HR (328 ± 24 vs. 331 ± 22 beats/min, P > 0.05).


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Results from this study support the conclusion that central AVP contributes, in part, to PEH. In this study, a single bout of dynamic exercise reduced postexercise AP and HR (Delta -21 ± 4 mmHg and Delta -20 ± 6 beats/min, respectively). This postexercise reduction in AP and HR is similar in magnitude to that recently reported for hypertensive rats (8, 9, 11, 29). Importantly, central administration of a selective AVP V1-receptor antagonist prevented postexercise reductions in AP and HR. The effect of AVP-X was limited to the central nervous system because the central dose used in this study (100 ng) (27) is significantly below that required for peripheral blockade (10-14 µg/kg) (39). Furthermore, central administration of AVP-X at rest did not significantly alter AP or HR. Similarly, sham exercise had no significant effect on resting AP or HR. Taken together, these data demonstrate that AVP, acting within the central nervous system, has a major role in the mechanisms mediating PEH.

Several investigators have reported a statistically and clinically significant reduction in resting AP and HR following a single bout of dynamic exercise in individuals and animals with hypertension (16, 28). The PEH is associated with elevations in cardiac output as well as reductions in peripheral resistance (22) and sympathetic nerve activity (20, 29). The postexercise sympathoinhibition is mediated by an enhanced inhibitory influence of the cardiopulmonary baroreflex as well as a decrease in gain and leftward shift of the arterial baroreflex function curve (9, 11).

It is well known that AVP modulates arterial and cardiopulmonary baroreflex function. Specifically, endogenously released AVP enhances the arterial and cardiopulmonary baroreflex inhibition of sympathetic nerve activity as well as reduces the gain and shifts the operating point of the arterial baroreflex to a lower pressure (23). AVP mediates its effect on baroreflex function through V1 vasopressin receptors in the central nervous system, specifically the area postrema. Thus it was reasonable to postulate that PEH may be mediated, in part, by AVP. Although the mechanisms responsible for the AVP-induced PEH were not investigated, several studies have reported that AVP activates neurons in the area postrema that project to the nucleus of the solitary tract (NTS) (Fig. 3A). These area postrema neurons sensitize NTS neurons to baroreceptor afferent signals. This response enhances processing of baroreceptor input (Fig. 3B) and resets the operating point of the arterial baroreflex to a lower pressure (Fig. 3C). Thus this effect of AVP is dependent on afferent input from peripheral baroreceptors (34). Importantly, it has been shown that sinoaortic denervation prevents PEH and sympathoinhibition in hypertensive rats (8). Furthermore, a single bout of dynamic exercise resets the operating point of the arterial baroreflex to lower pressures (9, 21). These data support a mechanism whereby AVP could mediate PEH by enhancing NTS responsiveness to baroreceptor input (37).


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  		Fig. 3.   Proposed model suggesting how an interaction between vasopressin (AVP) and the arterial and cardiopulmonary baroreflex mediates PEH. Endogenously released AVP activates neurons in the area postrema that project to the nucleus of the solitary tract (NTS; A). These area postrema neurons sensitize NTS neurons to baroreceptor afferent signals and enhance the inhibitory influence of the cardiopulmonary reflex such that for any baroreceptor activity at resting arterial pressure, NTS output is enhanced (B). In addition, the gain of the reflex is reduced such that for any change in arterial pressure, NTS output is reduced. In this model, the tonic increase in NTS activity resets the operating point to a lower pressure, reduces the gain of the arterial baroreflex, and mediates PEH (C).

An interesting and important question is how could the effects of AVP persist 60 min after the stimulus (exercise) for its release was completed? AVP has a systemic half-life of ~3-4 min. Although the half-life is probably longer in the central nervous system, it is reasonable to question how the effects of AVP could still be around 60 min after exercise. The mechanisms mediating the long-lasting effects of AVP [at least 60 min after the stimulus for its release (exercise) was completed] are unknown and were not investigated in this study. However, several investigators have reported a long-lasting effect of AVP in the central nervous system. For example, alterations in the HR response to dynamic exercise were observed 2 days after AVP was microinjected into the NTS of conscious rats (19). Furthermore, these investigators reported that repeated exposure to AVP (mediated by a daily exercise-induced release of AVP) caused a long-lasting sensitization to AVP. Similarly, central exposure to AVP potentiated the pressor (30) and behavioral (2, 36) responses to subsequent exposures to this peptide. This potentiation was mediated by V1 receptors and was reported to persist for days (36). Finally, AVP has a major role in memory (12), further supporting its long-lasting effects.

It has been suggested that the long-lasting effects of AVP were due to postreceptor mechanisms (15, 36) because no changes in V1-receptor density or affinity were observed. In addition, the long-lasting effect of AVP may be due, in part, to enhancing NTS responsiveness to baroreceptor input by a phenomenon termed "wind-up" (14, 18). Repetitive stimulation of unmyelinated baroreceptor afferents may result in hyperexcitability of NTS neurons via a poststimulatory facilitation mechanism (33). The influence of AVP on the poststimulatory facilitation mechanism ("wind-up") has not been investigated and merits further research.

In addition to the effect of AVP on the arterial baroreflex, this hormone also enhances the cardiopulmonary baroreflex regulation of the circulation. Specifically, endogenously released AVP enhances the reflex inhibitory response to activation of the cardiopulmonary baroreflex (24). Importantly, several studies have demonstrated that a single bout of dynamic exercise enhances the inhibitory influence of the cardiopulmonary baroreflex on the sympathetic nervous system (3, 11, 13). The postexercise facilitation of inhibitory cardiopulmonary baroreflexes may be due to AVP acting on the area postrema (Fig. 3A). In this situation, AVP could augment reflex sympathoinhibition in response to cardiopulmonary input and contribute, in part, to PEH.

Postexercise facilitation of inhibitory cardiopulmonary baroreflexes may also contribute to PEH by resetting the operating point of the arterial baroreflex to a lower pressure (5). Cardiopulmonary baroreflex afferents exert a tonic inhibitory influence on the arterial baroreflex such that the gain is reduced and the arterial baroreflex function curve is shifted to the left (10, 26). Furthermore, increasing cardiopulmonary baroreflex afferent activity further decreases the gain and shifts the arterial baroreflex function curve to the left (10). Thus the level of cardiopulmonary activity influences the gain and position of the arterial baroreflex function curve.

Limitations. With the use of the intracerebroventricular injection technique, we can only state that the effect is centrally mediated. Unfortunately, we cannot identify the specific central site(s) of action. In addition, it is possible that AVP-X is acting at multiple sites that have opposing responses. However, the intracerebroventricular injection technique is a reasonable first approach. Now that we are confident that the effect is centrally mediated, future investigations will focus on techniques for discrete microinjections into specific nuclei of conscious animals (19, 32).

Perspectives

AVP is a complex hormone that has multiple effects including water reabsorption at the distal and collecting tubules of the kidney as well as vascular smooth muscle constriction. Peripheral AVP also contributes to an increase in AP and redistribution of cardiac output during dynamic exercise via its vasoconstrictor actions (39-41). Importantly, AVP also interacts with arterial and cardiopulmonary baroreceptors to regulate cardiovascular function at rest and during exercise. Specifically, AVP acts at the area postrema to enhance arterial baroreflex-induced sympathoinhibition during static exercise (6). This effect of AVP may be due to a resetting of the operating point of the arterial baroreflex to a lower pressure. Resetting of the operating point of the arterial baroreflex to a lower pressure may be the same mechanism by which AVP mediates PEH. Specifically, AVP-induced facilitation of NTS processing of baroreceptor afferent input would mediate sympathoinhibition and shift the operating point of the arterial baroreflex to a lower pressure.


    ACKNOWLEDGEMENTS

This study was supported by the National Heart, Lung, and Blood Institute Grant HL-58414.


    FOOTNOTES

Address for reprint requests and other correspondence: S. E. DiCarlo, Dept. of Physiology, Wayne State Univ. School of Medicine, 540 E. Canfield Ave., Detroit, MI 48201 (E-mail: sdicarlo{at}med.wayne.edu).

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. Section 1734 solely to indicate this fact.

Received 27 November 2000; accepted in final form 29 March 2001.


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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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Am J Physiol Regul Integr Comp Physiol 281(2):R375-R380
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