| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Division of Cardiovascular Medicine, Department of Internal Medicine, and Department of Human Physiology, University of California, Davis, California 95616
 |
ABSTRACT |
|---|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
Circulating arginine vasopressin (AVP) can enhance baroreflex function via its action in the area postrema (AP). We tested the hypothesis that AVP acts in the AP to enhance baroreflex function during static contraction and, in turn, attenuates the exercise pressor reflex. Thus mean arterial blood pressure (n = 9) and heart rate (HR) (n = 9) during 30 s of electrically stimulated hindlimb contraction were compared before and after bilateral microinjections of 200 nl of the AVP V1-receptor antagonist d(CH2)5Tyr(Me)-AVP (V1x) (1 ng/nl) into the AP of the anesthetized cat. This protocol was repeated in three other cats in which sinoaortic denervation (SAD) was performed before any intervention. Injection of V1x into the AP had no effect on baseline blood pressure or HR. However, pressor and HR responses to static contraction were augmented by 44 ± 10 and 29 ± 9%, respectively. Static contraction also increased plasma AVP from 15.9 ± 2.0 to 25.5 ± 3.4 pg/ml. In the SAD cats, microinjection of V1x had no effect on contraction-induced increases in blood pressure or HR. These results suggest that baroreflex opposition of the reflex cardiovascular response to static contraction is enhanced by the action of AVP in the AP.
arterial baroreflex; static contraction; vasopressin V1 receptors
| |
INTRODUCTION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
THE CARDIOVASCULAR RESPONSE to static exercise is mediated, in part, by a reflex originating in contracting skeletal muscle (13). This reflex is often referred to as the "exercise pressor reflex" (16) and is characterized by increases in arterial blood pressure, heart rate, and sympathetic nerve activity (13, 27). The magnitude of these responses is modulated by the arterial baroreflex, which opposes the increases in blood pressure (29). The baroreflex, in turn, can be modulated by the central nervous system, particularly by the area postrema. This structure is a circumventricular organ located on the dorsomedial surface of the medulla just caudal to the fourth ventricle (31). Many neurons originating in this structure project into the nucleus tractus solitarius (NTS), where nerve endings of baroreceptor afferents also terminate (7, 17, 30). Consequently, the area postrema has been found to be an important modulator of baroreflex function (1, 8, 26).
The fact that the area postrema is not protected by the blood-brain barrier suggests that the interaction between area postrema and NTS neurons may be influenced by substances circulating in the blood such that baroreflex function is altered. One substance of particular interest is arginine vasopressin (AVP), which has been shown to enhance baroreflex function via activation of AVP V1 receptors in the area postrema (1, 8, 22, 26). Because plasma AVP increases during episodes of static muscle contraction (18), it may also enhance baroreflex function during exercise. Supporting this possibility are the observations that chemical lesion of cell bodies in the area postrema (3) or intravenous administration of a V1-receptor antagonist (23) enhances cardiovascular responses to static contraction, presumably by attenuating baroreflex inhibition.
We have extended these studies by examining the effects of V1-receptor blockade on the exercise pressor reflex when a V1 blocker was applied directly to the area postrema. We hypothesized that the exercise pressor reflex is augmented by V1-receptor inhibition in the area postrema and that this effect is dependent on an intact arterial baroreflex.
| |
METHODS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
Surgical Preparation
Experiments were performed on 40 adult cats of either sex (weight 2.5-4.5 kg). All protocols were approved by the Animal Use and Care Administrative Advisory Committee, University of California, Davis, and were in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals [Department of Health and Human Services Publication No. (NIH) 85-23, Revised 1985]. Each cat was initially anesthetized by intramuscular injection of ketamine (25-40 mg/kg) followed by bolus intravenous injections of
-chloralose (total dose, 70-100
mg/kg). All cats were intubated and placed on positive-pressure
ventilation (Harvard Apparatus). Catheters were placed in the left
femoral vein for administering drugs or fluids and in the left femoral
artery for measuring arterial blood pressure. Arterial pressure was
measured with a pressure transducer (Statham P23 ID) attached to the
arterial catheter. Arterial blood gases and pH were evaluated
periodically using an ABL3 blood gas analyzer (Radiometer, Copenhagen,
Denmark) and were maintained within the following ranges:
PCO2, 25-35 mmHg;
PO2, >90 mmHg; pH, 7.35-7.44.
Values outside these ranges were corrected by enriching the inspired
air with oxygen, administering intravenous sodium bicarbonate (1.5%
solution), and/or adjusting ventilation.
Static Hindlimb Contractions
Isometric (static) contractions of the right hindlimb were produced by placing the cats in a David Kopf spinal unit and pinning the hips at the level of the iliac crest. The limb was then fully extended and fixed in position by clamping the ankle. To measure the force of contraction in the triceps surae muscle, the Achilles tendon was separated from the calcaneus bone and then attached to an isometric force transducer (Grass FT-10). The muscle was contracted neurogenically by electrically stimulating the right tibial nerve. The nerve was dissected free of surrounding tissue and then placed on bipolar silver-wire electrodes. The electrodes were connected to a constant-current stimulus isolation unit (Grass PSIU6) and square-wave stimulator (Grass S88). The nerve was stimulated with pulses of 0.025-ms duration at a voltage amplitude of 1.8-2.0 times motor threshold. These parameters were used because they avoided direct activation of group III and IV afferent fibers within the tibial nerve, which could contribute to the cardiovascular response produced by contraction (4, 21). Finally, the stimulus frequency was set at 40 Hz to produce a smooth tetanic contraction over 30 s.Microinjections Into the Area Postrema
A craniotomy was performed to expose the area postrema. Briefly, the cat's head was placed in a stereotaxic frame (David Kopf) with the head rotated forward ~45°. A midline incision was made from the lamboidal ridge to the second cervical vertebra, and the overlying muscles were removed from the occipital bone to the first cervical vertebra. The occipital bone was cut away, and the atlantooccipital ligament and arachnoid membrane were removed. To view the brain stem, the cerebellum was then retracted forward using a customized clamp. Finally, the dura was peeled from the surface of the area postrema. Microinjections into the area postrema were made using a pneumatic picospritzer (General Valve: pressure, 3-50 lb/in.2). A single- or double-barreled micropipette (outside tip diameter 10-25 µm) was attached to a micromanipulator (David Kopf) and positioned over the area postrema. The pipette tip was inserted into the area postrema to a depth of 100-1,000 µm. AVP or a V1-receptor antagonist was injected in solution with Chicago sky blue dye so that distribution of the injectate could be later determined histologically. The volume of each injection was determined using a customized tubing system. A partially filled noncompressible tube (PE-160) was connected to the fully loaded pipette and was positioned such that the fluid meniscus was visible on a microscope stage. The distal end of the tube was then attached to the picospritzer. A calibrated reticule in the microscope was used to measure the positional change of the meniscus, which was converted to the volume of fluid injected (1 division = 6.2 nl).Denervations
To remove baroreceptor afferent input, bilateral sinoaortic denervation (SAD) was performed in some animals. A ventral midline incision was made in the neck, and the underlying muscles were dissected to expose the common, internal, and external carotid arteries bilaterally. These arteries and the carotid sinus were stripped of all visible nerves, and the carotid and vagus nerves were cut bilaterally. The area was then treated with 10% phenol.Measurement of AVP
In cats in which plasma AVP was measured, surgical exposure of the area postrema was not performed. Samples of arterial blood were collected in tubes containing 100 µl EDTA and centrifuged at 3,000 g for 10 min at 4°C, and then the plasma was stored at
70°C.
AVP was extracted from the plasma by adsorption onto octadecylsilyl columns (Sep-Pak, C18) at a pH of 2-3. Columns were prepared by washing with 5 ml methanol, 5 ml urea (8 M), and 10 ml distilled water. After the plasma passed through, each column was washed with 10 ml of 4% acetic acid and 10 ml distilled water and then eluted with 10 ml of 90% ethanol (6% water and 4% acetic acid). An RIA was performed on the extracted plasma using rabbit antiserum that is highly specific for AVP, cross-reacts 100% with lysine vasopressin, and does not cross-react with angiotensin I or II, oxytocin, or vasotocin. Standards were prepared using AVP (Bachem, Torrance, CA) and 125I-labeled [Tyr2,Arg8]AVP (New England Nuclear, Boston, MA). The coefficient of variation within assays was 2%, and the lower limit of detection was 1 pg/ml.
Protocols
In every protocol involving AVP V1-receptor blockade, at least two static contractions, 30 min apart, were performed before any intervention to demonstrate the presence of a repeatable cardiovascular response (24). The criterion for the presence of the exercise pressor reflex was an increase in blood pressure of at least 15 mmHg.AVP V1-receptor blockade in the area postrema. In nine cats, mean arterial pressure and heart rate responses to 30 s of electrically stimulated static contraction of the hindlimb were compared before and 30-45 min after bilateral microinjection of the selective AVP V1-receptor antagonist d(CH2)5Tyr(Me)-AVP (V1x) (11) into the area postrema. The V1-receptor antagonist V1x was mixed with 0.9% saline and 5% Chicago sky blue dye to produce a final antagonist concentration of 1 ng/nl (final dye concentration 2.5%). Because the cat area postrema is a V-shaped bilateral structure, two microinjections were made into each side to optimize distribution of the drug. Each injection was 40-50 nl, yielding a total of 160-200 nl. In previous volume control studies, we found that neither the volume of injectate (200-250 µl) nor the vehicle for the antagonist (the 5% solution of Chicago sky blue dye) had any effect on the exercise pressor reflex (3). Efficacy of V1-receptor blockade was determined by a >70% reduction in the pressor response to microinjection of 20 ng AVP into the area postrema.
To determine if V1x could diffuse from the area postrema into the general circulation to cause a systemic effect, we repeated the previous protocol with the exception that the total dose of the V1-receptor antagonist (200 ng) was injected intravenously rather than into the area postrema (n = 3). Because surgery and anesthesia may have caused increases in circulating AVP, a potential problem was that elevated baseline levels of this peptide could add to those produced during static contraction and, in turn, contribute to modulation of the exercise pressor reflex. To examine this potential effect, we used phenylephrine to increase mean arterial pressure to a degree similar to that observed during static contraction, but without causing the concomitant increase in AVP. We performed the same surgery as in the microinjection protocols and then injected phenylephrine intravenously (1-5 µg) before and after intravenous injection of 10-15 µg/kg V1x (n = 4 cats). We chose phenylephrine for its ability to produce repeatable pressor responses over the required time course and because it has no known direct effects on plasma AVP. At least two injections of phenylephrine were made before V1-receptor blockade to demonstrate repeatability of the pressor response. We chose an intravenous dose of 10-15 µg/kg V1x because it is capable of augmenting the exercise pressor response independent of any vascular effects of AVP (23).AVP V1-receptor blockade in SAD cats. This protocol was performed to determine if the effects of AVP in the area postrema were dependent on an intact arterial baroreflex. Subsequent to SAD, mean arterial pressure and heart rate responses to 30 s of static contraction were assessed before and after bilateral injection of V1x into the area postrema, as previously described (n = 3). This protocol was repeated in four additional cats, with the exception that V1x (10-15 µg/kg) was injected intravenously.
In all cats, efficacy of SAD was confirmed by a >75% reduction in the pressor response to bilateral clamping of the common carotid arteries caudal to their bifurcations.AVP V1-receptor blockade in the NTS. To determine any possible effects of antagonist migration from the area postrema into the NTS, the cardiovascular response to 30 s of static contraction was compared before and after bilateral injection of V1x into the NTS (n = 5). These injections (two 50-nl injections into the right and left NTS) were made immediately lateral to the area postrema.
Plasma AVP Concentrations During Static Contraction
To confirm that 30 s of electrically stimulated static contraction causes increases in plasma AVP, arterial blood samples were obtained for measurement of this hormone (n = 10). One sample was withdrawn 1-2 min before contraction, and the second sample was taken immediately after contraction. Each sample contained 1 ml of blood withdrawn from the femoral artery catheter.Histology
At the end of each experiment, the brain stem was excised and then fixed in a solution of 4% paraformaldehyde and 10% sucrose for at least 48 h. Next, the tissue was trimmed and mounted on a frozen cryostat block using Tissue-Tek OCT compound (Miles) and stored at70°C for at least 24 h. Frozen coronal sections (40-80
µm thick) were then sliced in a cryostat and placed on chromium
gelatin-coated slides. Verification of the distribution of the dye was
determined by light microscopy.
Deletion of Animals
Two cats were deleted from analysis. One was eliminated because dye was observed in the area postrema on the right side but in the NTS on the left side. The other cat was removed because the amount of time between the last control contraction and the contraction subsequent to microinjection of V1x into the area postrema (>65 min) was not comparable to that of the other cats in this protocol (30-45 min). Moreover, dye could not be located in any of our frozen sections of the brain stem.Drugs
AVP and V1x (Bachem, Torrance, CA) were dissolved in Milli-Q water to form a stock solution of 1 mg/ml. Subsequent dilutions were made with 0.9% saline and 5% Chicago blue dye to obtain the final concentration of 100 pg/ml for AVP and 1 ng/nl for V1x. Chicago blue dye (Sigma Chemical, St. Louis, MO) was dissolved with 0.5 mM sodium acetate to produce a 5% stock solution, and the pH was adjusted to 7.3-7.4. All solutions were filtered before injection.Data Analysis
The tension developed during static contraction was calculated as the difference between peak tension and resting tension.Statistics
Results are expressed as means ± SE. Because we found that much of our data were skewed and/or had more than one peak, we made the assumption that they were not normally distributed. Consequently, a nonparametric statistical analysis was performed. Comparisons between two means were made using the Wilcoxon signed-rank test. Multiple comparisons were performed using Friedman's randomized block analysis of variance followed by the Student-Newman-Keuls post hoc analysis of the ranked sums. Differences between means were judged to be significantly different at P < 0.05.| |
RESULTS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
Effects of Static Contraction on Plasma AVP
Static contraction caused the concentration of plasma AVP to increase from 15.9 ± 2.0 to 25.5 ± 3.4 pg/ml (P < 0.05). In addition, muscle tension (evoked by the same stimulus parameters used throughout the study) increased from 0.3 ± 0.1 to 2.3 ± 0.3 kg (P < 0.05). The change in tension (2 kg) was typical of those observed in the subsequent protocols.Effects of AVP V1-Receptor Antagonism in the Area Postrema
Compared with control conditions, increases in blood pressure and heart rate during static contraction were greater after microinjection of V1x into the area postrema (Figs. 1 and 2). Peak muscle tension was not different between conditions.
|
|
Intravenous injection of the same dose of V1x that was injected into the area postrema had no effect on contraction-evoked increases in blood pressure or heart rate (Table 1).
|
The pressor response to unilateral injection of 20 ng AVP into the area postrema was practically eliminated by blockade of AVP V1 receptors in this structure. Initially, AVP injection caused an increase in blood pressure of 18 ± 2 mmHg. After microinjection of V1x, the AVP-evoked pressor response was only 4 ± 1 mmHg.
In the phenylephrine protocol, the initial pressor response to intravenous injection of 1-5 µg of this vasoconstrictor was 46 ± 8 mmHg. Subsequent to intravenous injection of V1x, the pressor response was marginally enhanced (50 ± 9 mmHg). However, enhancement occurred in all four cats and was statistically significant (P < 0.05).
Effects of SAD and AVP V1-Receptor Blockade
SAD abolished the pressor and heart rate responses to bilateral carotid artery occlusion. Before SAD, occlusion increased blood pressure by 29 ± 5 mmHg and heart rate by 10 ± 6 beats/min. After SAD, occlusion caused increases in blood pressure and heart rate of only 5 ± 4 mmHg and 0 ± 1 beats/min, respectively. SAD also caused an increase in baseline blood pressure (106 ± 11 vs. 118 ± 11 mmHg) that lasted for at least 30 min. After SAD was confirmed, microinjection of V1x into the area postrema or into the systemic circulation had no effect on the blood pressure, heart rate, or muscle tension responses to static contraction (Table 1).Effects of AVP V1-Receptor Blockade in the Medial NTS
When contraction-induced increases in blood pressure and heart rate were compared before and after bilateral microinjection of V1x into the medial border regions of the NTS, no significant differences were observed (Table 1). Peak muscle tension was also unchanged.| |
DISCUSSION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
The general findings of this investigation support our contention that AVP acts in the area postrema to attenuate the exercise pressor reflex. First, microinjection of the selective AVP V1-receptor antagonist V1x into the area postrema augmented increases in mean arterial pressure and heart rate during static contraction. Second, plasma AVP increased during the 30-s period of static contraction used in this investigation. Thus the most noteworthy observation in this study was that in vivo concentrations of AVP, produced by short-duration static contraction, were capable of reducing the exercise pressor reflex.
Another important finding of this study was that the augmentation of the exercise pressor reflex during AVP V1-receptor blockade was dependent on an intact arterial baroreflex. Although an intact arterial baroreflex is believed to be essential to AVP actions in the area postrema (1, 22), at least one study has reported that effects of AVP injection into the area postrema (i.e., inhibition of sympathetic nerve activity) can occur in the absence of baroreceptor input (i.e., SAD) (25). However, another investigation using the same animal model (rabbit) has clearly demonstrated that progressive SAD diminishes the capability of AVP to suppress renal sympathetic nerve activity (RSNA) (19). Although the reasons for these differential findings are not clear, our results support those of the latter study. We failed to see any contraction-induced augmentation of blood pressure during AVP V1-receptor blockade when SAD was performed before the initiation of the contraction protocols. This was the case whether V1x was given intravenously at a dose capable of enhancing the exercise pressor reflex in baroreflex-intact cats (23) or whether it was injected directly into the area postrema. Thus it is reasonable to assume that AVP acts in the area postrema during muscle contraction to enhance baroreflex function.
The effects of V1x reported in this study were not due to diffusion of the antagonist into the systemic circulation or its migration into surrounding areas of the CNS. We found that intravenous injection of the 200-ng dose of V1x had no effect on the exercise pressor reflex. Furthermore, we excluded from the study any cat in which the Chicago blue dye was observed outside the confines of the area postrema. We also demonstrated that microinjection of V1x into the medial border region of the NTS, adjacent to the area postrema, had no effect on the exercise pressor reflex. This observation suggests that if V1x had migrated from the area postrema into the NTS, it did not affect the outcome of our study. This is an important finding because antagonism of V1 receptors in the NTS can evoke AVP-induced attenuation of baroreflex control of blood pressure and RSNA under certain circumstances (e.g., when microinjections of V1x are made into the more caudal portion of the NTS) (9). In view of these results, we concluded that the action of V1x on the exercise pressor reflex was limited to the area postrema.
The amount of V1x needed to achieve AVP V1 receptor blockade in the area postrema was based on results of an earlier investigation in rabbits (8). In that study, microinjection of 100 ng V1x into the area postrema abolished the ability of AVP to augment baroreflex inhibition of RSNA. Although the size of the rabbits was similar to that of the cats used in the present study, the area postrema is a unilateral structure in rabbits and bilateral in cats. Consequently, we injected 100 ng V1x into each side of the cat area postrema. Because this dose virtually abolished the pressor response to unilateral injection of AVP into the area postrema, we reasoned that effective V1-receptor blockade had been achieved.
Past investigation has revealed that the area postrema is capable of attenuating the exercise pressor reflex (3). In this regard, chemical lesion of cell bodies in the area postrema caused an augmention of static contraction-induced pressor and heart rate responses of 57 and 42%, respectively (3). In the present study, antagonism of V1 receptors in the area postrema increased the blood pressure response to contraction by 44 ± 10% and the concomitant heart rate response by 29 ± 9%. Thus it appears that AVP plays a major role in area postrema-evoked modulation of the exercise pressor reflex.
The manner in which AVP modulates the exercise pressor reflex is not completely clear. However, there is evidence to suggest that the action of this peptide in the area postrema enhances the ability of the arterial baroreflex to attenuate sympathetic outflow (1, 8, 22, 26). This attenuation is believed to be the result of a resetting of the baroreflex threshold to lower arterial pressures (1). If this same phenomenon also occurs during static contraction, then the mechanism most likely underlying these effects of AVP is excitation of neurons in the area postrema that project into the NTS. In the NTS, these area postrema neurons form excitatory convergent synapses with baroreceptor afferents and NTS neurons and, thereby, facilitate processing of baroreceptor input into the NTS (2, 5). This contention is supported by indirect evidence from a recent study (22) in which baroreflex-induced (i.e., phenylephrine infusion) decreases in lumbar sympathetic nerve activity and hindquarters resistance were augmented by concurrent intravertebral infusion of AVP (performed to maximize delivery of this hormone to the area postrema).
Our findings suggesting that AVP enhances baroreflex function during exercise appear to be at odds with results of studies indicating that the baroreflex is reset to higher systemic blood pressures at the onset of muscle contraction (14, 15). This resetting is caused by inhibition of the vagal component of the reflex via activation of group III and IV muscle afferents. However, our data do not preclude an upward resetting of the baroreflex; they merely suggest that its function can be modulated by AVP. Although the reason for this modulation is not obvious, it may enable the baroreflex to minimize increases in blood pressure that would exceed those that are necessary to adequately perfuse the contracting muscle. This series of events would tend to optimize the work of the heart.
Experimental Limitations
Even though 30 s of static contraction increased plasma concentrations of AVP, it should be noted that our baseline level (15.9 ± 2.0 pg/ml) was somewhat higher than those in conscious, unrestrained cats (6.3-8.5 pg/ml) (12, 20). This elevation was probably due to inherent effects of surgery and/or anesthesia, both of which can cause the release of AVP (6). This outcome raises the issue that V1x-induced augmentation of the exercise pressor reflex may have been due to inhibition of the action of circulating levels of AVP produced by the combined effects of muscle contraction and surgery/anesthesia. The fact that the pressor response to intravenous injection of phenylephrine was enhanced by V1- receptor blockade supports this possibility. However, this augmentation was small (46 ± 8 vs. 50 ± 9 mmHg). Therefore, it is not unreasonable to presume that the acute increase in plasma AVP caused by static contraction was an important factor underlying augmentation of the exercise pressor reflex during V1-receptor blockade.We did not determine the stimuli responsible for the contraction-induced release of AVP. Effects of important factors such as body temperature, plasma volume, and plasma osmolality (28) were probably minimal, because 30 s of contraction likely would have caused only small changes in these variables. However, it has been reported that short bouts of contraction activate group III and IV muscle afferents to cause increases in the activity of AVP- and oxytocin-containing supraoptic nucleus neurons that project to the pituitary gland (10). Thus a major portion of AVP release during contraction in this study may have been caused by a neuroendocrine reflex originating in active skeletal muscle.
In conclusion, injection of the AVP V1-receptor antagonist V1x into the area postrema increased arterial blood pressure and heart rate in response to static contraction. This augmentation did not occur in cats that underwent baroreceptor afferent denervation (SAD). Taken together, these data suggest that AVP acts in the area postrema during muscle contraction to enhance baroreflex-induced opposition of the exercise pressor reflex. It is possible that AVP modulates the arterial baroreflex to prevent contraction-induced increases in blood pressure from surpassing those necessary for sufficient perfusion of the active skeletal muscle and, in turn, minimize the work of the heart.
| |
ACKNOWLEDGEMENTS |
|---|
This work was supported by National Heart, Lung, and Blood Institute Grant HL-48373.
| |
FOOTNOTES |
|---|
These results were presented, in part, at the annual meeting of Experimental Biology, New Orleans, LA, in April 1997.
Address for reprint requests: C. Stebbins, Div. of Cardiovascular Medicine, TB 172, Univ. of California, Davis, CA 95616-8634.
Received 14 August 1997; accepted in final form 25 February 1998.
| |
REFERENCES |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
1.
Bishop, V. S.,
and
M. Hay.
Involvement of the area postrema in the regulation of sympathetic outflow to the cardiovascular system.
Front. Neuroendocrinol.
14:
57-75,
1993[Medline].
2.
Bonham, A. C.,
and
E. M. Hasser.
Area postrema and aortic or vagal afferents converge to excite cells in nucleus tractus solitarius.
Am. J. Physiol.
264 (Heart Circ. Physiol. 33):
H1674-H1685,
1993
3.
Bonigut, S.,
A. C. Bonham,
and
C. L. Stebbins.
Area postrema-induced inhibition of the exercise pressor reflex.
Am. J. Physiol.
272 (Heart Circ. Physiol. 41):
H1650-H1655,
1997
4.
Bonigut, S.,
C. L. Stebbins,
and
J. C. Longhurst.
Reactive oxygen species modify the reflex cardiovascular response to static contraction.
J. Appl. Physiol.
81:
1207-1212,
1996
5.
Cai, Y.,
M. Hay,
and
V. S. Bishop.
Stimulation of area postrema by vasopressin and angiotensin II modulates neuronal activity in the nucleus tractus solitarius.
Brain Res.
647:
242-248,
1994[Medline].
6.
Corman, B.,
and
G. Geelen.
Effects of blood sampling, anesthesia, and surgery on plasma vasopressin concentrations in the rat.
Experientia
48:
268-270,
1992[Medline].
7.
Cottle, M. K.
Degeneration studies of primary afferents of IXth and Xth cranial nerves in the cat.
J. Comp. Neurol.
122:
329-345,
1964[Medline].
8.
Hasser, E. M.,
and
V. S. Bishop.
Reflex effect of vasopressin after blockade of V1 receptors in the area postrema.
Circ. Res.
67:
265-271,
1990
9.
Hegarty, A. A.,
and
R. B. Felder.
Antagonism of vasopressin V1 receptors in NTS attenuates baroreflex control of renal nerve activity.
Am. J. Physiol.
269 (Heart Circ. Physiol. 38):
H1080-H1086,
1995
10.
Kannan, H.,
H. Yamashita,
K. Koizumi,
and
C. M. Brooks.
Neuronal activity of the cat supraoptic nucleus is influenced by muscle small-diameter afferent (groups III and IV) receptors.
Proc. Natl. Acad. Sci. USA
85:
5744-5748,
1988
11.
Kruszynski, M.,
B. Lammek,
and
M. Manning.
[1-(Mercapto-
,-cyclopentamethylenepropionic acid),2-(0-methyl)tyrosine]arginine-vasopressin and 1-(-mercapto-,-cyclopentamethylenepropionic acid)arginine-vasopressin, two highly potent antagonists of the vasopressor response to arginine-vasopressin.
J. Med. Chem.
23:
364-368,
1980[Medline].
12.
Martin, D. S.,
and
J. R. McNeill.
Pressor and intestinal vascular bed responses to vasopressin after cholinergic blockade.
Am. J. Physiol.
254 (Heart Circ. Physiol. 23):
H45-H51,
1988
13.
McCloskey, D. I.,
and
J. H. Mitchell.
Reflex cardiovascular and respiratory responses originating in exercising muscle.
J. Physiol. (Lond.)
224:
173-186,
1972
14.
McWilliam, P. N.,
and
T. Yang.
Inhibition of cardiac vagal component of baroreflex by group III and IV afferents.
Am. J. Physiol.
260 (Heart Circ. Physiol. 29):
H730-H734,
1991
15.
McWilliam, P. N.,
T. Yang,
and
L. X. Chein.
Changes in baroreceptor reflex by muscle contraction in the decerebrate cat.
J. Physiol. (Lond.)
436:
549-558,
1991
16.
Mitchell, J. H.,
M. P. Kaufman,
and
G. A. Iwamoto.
The exercise pressor reflex: its cardiovascular effects, afferent mechanisms, and central pathways.
Annu. Rev. Physiol.
45:
229-242,
1983[Medline].
17.
Morest, D. K.
Experimental study of the projections of the nucleus of the tractus solitarius and the area postrema.
J. Comp. Neurol.
130:
227-300,
1967.
18.
Nazar, K.,
D. Jezová,
and
E. Kowalik-Borowka.
Plasma vasopressin, growth hormone and ACTH responses to static handgrip in healthy subjects.
Eur. J. Appl. Physiol.
58:
400-404,
1989.
19.
Nishida, Y.,
and
V. S. Bishop.
Vasopressin-induced suppression of renal sympathetic outflow depends on the number of baroafferent inputs in rabbits.
Am. J. Physiol.
263 (Regulatory Integrative Comp. Physiol. 32):
R1187-R1194,
1992
20.
Reaves, T. A., Jr.,
H.-M. Liu,
M. M. Qasim,
and
J. N. Hayward.
Osmotic regulation of vasopressin in the cat.
Am. J. Physiol.
240 (Endocrinol. Metab. 3):
E108-E111,
1981
21.
Rybicki, K. J.,
and
M. P. Kaufman.
Stimulation of group III and group IV afferents reflexly decreases total pulmonary resistance in dogs.
Respir. Physiol.
59:
185-189,
1985[Medline].
22.
Scheuer, D. A.,
and
V. S. Bishop.
Effect of vasopressin on baroreflex control of lumbar sympathetic nerve activity and hindquarter resistance.
Am. J. Physiol.
270 (Heart Circ. Physiol. 39):
H1963-H1971,
1996
23.
Stebbins, C. L.
Reflex cardiovascular response to exercise is modulated by circulating vasopressin.
Am. J. Physiol.
263 (Regulatory Integrative Comp. Physiol. 32):
R1104-R1109,
1992
24.
Stebbins, C. L.,
A. Ortiz-Acevedo,
and
J. M. Hill.
Spinal vasopressin modulates the reflex cardiovascular response to static contraction.
J. Appl. Physiol.
72:
731-738,
1992
25.
Suzuki, S.,
A. Takeshita,
T. Imaizumi,
Y. Hirooka,
M. Yoshida,
S. Ando,
and
M. Nakamura.
Central nervous system mechanisms involved in inhibition of renal sympathetic nerve activity induced by arginine vasopressin.
Circ. Res.
65:
1390-1399,
1989
26.
Undesser, K. P.,
E. M. Hasser,
J. R. Haywood,
A. K. Johnson,
and
V. S. Bishop.
Interaction of vasopressin with the area postrema in arterial baroreflex function in conscious rabbits.
Circ. Res.
56:
410-417,
1985
27.
Victor, R. G.,
D. M. Rotto,
S. L. Pryor,
and
M. P. Kaufman.
Stimulation of renal sympathetic activity by static contraction: evidence for mechanoreceptor-induced reflexes from skeletal muscle.
Circ. Res.
64:
592-599,
1989
28.
Wade, C. E.
Response, regulation, and actions of vasopressin during exercise: a review.
Med. Sci. Sports Exerc.
16:
506-511,
1984[Medline].
29.
Waldrop, T. G.,
and
J. H. Mitchell.
Effects of barodenervation on cardiovascular responses to static muscular contraction.
Am. J. Physiol.
249 (Heart Circ. Physiol. 18):
H710-H714,
1985
30.
Wallach, A.,
and
A. D. Loewy.
Projections of the aortic nerve to the nucleus tractus solitarius in the rabbit.
Brain Res.
188:
247-251,
1980[Medline].
31.
Wislocki, G. B.,
and
T. J. Putnam.
Note on the anatomy of the area postrema.
Anat. Rec.
19:
281-287,
1920.
This article has been cited by other articles:
|
|
 |
|
  H. L. Collins, D. W. Rodenbaugh, and S. E. DiCarlo Central blockade of vasopressin V1 receptors attenuates postexercise hypotension Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2001; 281(2): R375 - R380. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
) in mean arterial pressure (MAP), heart rate (HR),
and developed tension (tension) in response to static hindlimb
contraction before (open bars) and after (solid bars) bilateral
microinjection of
d(CH2)5Tyr(Me)-arginine
vasopressin (200 ng) into area postrema. Values are means ± SE;
numbers below bars are control values.
* P < 0.05 vs. control.