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Am J Physiol Heart Circ Physiol 284: H1003-H1007, 2003. First published November 21, 2002; doi:10.1152/ajpheart.00793.2002
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Vol. 284, Issue 3, H1003-H1007, March 2003

Role of the area postrema in angiotensin II modulation of baroreflex control of heart rate in conscious mice

Baojian Xue, Hope Gole, Jaya Pamidimukkala, and Meredith Hay

Dalton Cardiovascular Research Center and Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

This study reports the effects of angiotensin II (ANG II), arginine vasopression (AVP), phenylephrine (PE), and sodium nitroprusside (SNP) on baroreflex control of heart rate in the presence and absence of the area postrema (AP) in conscious mice. In intact, sham-lesioned mice, baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of ANG II were significantly less than those observed with similar increases in arterial pressure with PE (slope: -3.0 ± 0.9 vs. -8.1 ± 1.5 beats · min-1 · mmHg-1). Baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of AVP were the same as those observed with PE in sham animals (slope: -5.8 ± 0.7 vs. -8.1 ± 1.5 beats · min-1 · mmHg-1). After the AP was lesioned, the slope of baroreflex inhibition of heart rate was the same whether pressure was increased with ANG II, AVP, or PE. The slope of the baroreflex-induced increases in heart rate due to decreases in arterial blood pressure with SNP were the same in sham- and AP-lesioned animals. These results indicate that, similar to other species, in mice the ability of ANG II to acutely reset baroreflex control of heart rate is dependent on an intact AP.

vasopressin; autonomic nervous system; circumventricular organs


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

THE AREA POSTREMA (AP) is a circumventricular organ in the medulla that is subject to modulation by both neural and humoral factors. Chemical activation of the AP has been shown to be involved in a number of physiological functions, including taste sensitivity, emesis, and cardiovascular regulation (6, 7, 14, 16, 40). Some peptide hormones are believed to exert their central effects primarily through actions at neurons within the AP. Neurons within the AP are known to be activated and express receptors for a number of different neuropeptides, including angiotensin II (ANG II) and arginine vasopressin (AVP) (10, 24, 25).

Substantial evidence has been accumulated suggesting that circulating vasoactive peptides such as ANG II and AVP act at the AP to modulate sympathetic and vagal activity and ultimately baroreflex regulation of blood pressure (2, 4, 23). In a number of different species, ANG II is known to increase arterial blood pressure while blunting baroreflex-induced bradycardia (11, 18, 29). The mechanism underlying this effect of ANG II is thought to be due to a central action of ANG II to increase vagal withdrawal and/or increase sympathetic outflow (11, 28, 32, 34, 35). In contrast to ANG II, AVP has been shown in some species to facilitate sympathoinhibition and shift baroreflex control of the sympathetic nervous system to lower pressures (12, 21, 36, 40, 41). The central site thought to be involved in the modulation of the baroreflex control of heart rate by ANG II and AVP is the AP (12, 18, 29, 31).

There is currently a vast array of transgenic mice models that can be used to facilitate our understanding of central mechanisms regulating cardiovascular function. However, the role of the AP in neurohumoral regulation of cardiovascular function in mice has not been determined. The purpose of the present study was to determine the role of the AP in ANG II and AVP modulation of baroreflex control of heart rate in conscious mice.


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

All experiments were carried out in c57 strain wild-type male mice. These mice were a gift from Dr. Dennis Lubahn (University of Missouri, Columbia, MO). The experiment was composed of the experimental group of AP-lesioned mice and the control group of AP sham-lesioned mice.

AP lesion. Mice (6-7 mo old) were anesthetized with a mixture of ketamine (100 mg/kg) and xylazine (10 mg/kg) supplemented with isofluorane when necessary. The AP was exposed by opening the atlantoocipital membrane and was removed using vacuum aspiration. The AP sham-lesioned mice underwent the same procedure except that the AP was not removed. At the end of the experiment, the animals were euthanized and perfused. The accuracy of the AP lesions and AP sham lesions was verified histologically.

Instrumentation. The mice were instrumented with chronic arterial and venous catheters 4 mo postAP lesion surgery. Animals were anesthetized as described above. Arterial and venous catheters constructed of Micro-Renathane tubing [MRE-025, 0.64 mm outer diameter (OD), 0.30 mm inner diameter (ID), Braintree Scientific] were chronically implanted into the femoral artery and vein for the measurement of arterial pressure and administration of drugs, respectively. The free ends of these catheters were tunneled subcutaneously and exteriorized at the back of the neck. Catheters were then threaded through polyethylene tubing (2.80 mm OD, 1.77 mm ID, Becton-Dickinson). The tubing was secured with sutures. The experiments were carried out in conscious, freely moving mice 4-5 days after surgery.

Evaluation of cardiac baroreflexes. Arterial blood pressure was recorded with a MLT0698 disposable blood pressure transducer. Heart rate and mean arterial pressure (MAP) were derived by data-acquisition software (Powerlab) using the arterial pressure pulse. Cardiac baroreflexes were evoked by increasing arterial pressures with ramp infusions of either phenylephrine (PE; 1.0 mg/ml), ANG II (100 µg/ml), or AVP (25 µM) and by lowering blood pressure with sodium nitroprusside (SNP; 1.0 mg/ml). Infusion rates (0.003 ml/min) were monitored such that blood pressure was increased or decreased 30-40 mmHg over a 30- to 45-s period. The drug order was randomized, and 45-60 min were allowed between each curve.

Statistical analysis. Data are presented as means ± SE. Statistical significance was determined using a paired t-test or two-way ANOVA where needed. To analyze baroreflex responses, the absolute value of heart rate for each dose of ANG II, AVP, PE , or SNP was plotted against the corresponding value of MAP for each mouse, and the data were subjected to linear regression analysis. A value of P < 0.05 was considered to be statistically significant.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Resting values for blood pressure and heart rate were not significantly different between sham (n = 8, 122 ± 2 mmHg and 691 ± 20 beats/min) and lesioned animals (n = 10, 120 ± 4 mmHg and 679 ± 16 beats/min) (Fig. 1).


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  		Fig. 1.   Resting mean arterial blood pressure (MAP; in mmHg) and heart rate (HR; in beats/min) in male mice with intact (sham; n = 8) or lesioned area postremas (APX; n = 10). Resting values for MAP and HR were not significantly different between sham and APX mice (P > 0.05).

The linear regression analysis of the heart rate baroreflex responses to intravenous infusions of ANG II and PE in sham- and AP-lesioned mice are shown in Fig. 2 and Table 1. In sham-lesioned animals, the slope of the line for the ANG II-induced heart rate response was -3.0 ± 0.9 beats · min-1 · mmHg-1 and was significantly less than that observed with PE (-8.1 ± 1.5 beats · min-1 · mmHg-1). In AP-lesioned animals, the slope of the line for the ANG II-induced heart rate (-7.2 ± 1.0 beats · min-1 · mmHg-1) was the same as that observed with PE (-7.7 ± 1.0 beats · min-1 · mmHg-1).


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  		Fig. 2.   Reflex bradycardia responses to angiotensin II (ANG II) compared with phenylephrine (PE). The graph shows regression lines relating baroreflex inhibition of HR (in beats/min) to increases in MAP (in mmHg) with PE and ANG II in sham (A, n = 8) or APX mice (B, n = 10). Values are means ± SE. * Significant difference compared with PE (P < 0.05).


                              
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  		Table 1.   Slopes of baroreflex responses to PE, ANG II, AVP, and SNP in male mice with an intact or lesioned area postremas

Figure 3 illustrates the linear regression analysis of the heart rate baroreflex responses to intravenous AVP (Fig. 3 and Table 1) in sham- and AP-lesioned animals. In sham-lesioned animals, the slope of the line for the AVP-induced heart rate response was -5.8 ± 0.7 beats · min-1 · mmHg-1, which was similar to that observed in the AP-lesioned animals (-6.1 ± 1.0 beats · min-1 · mmHg-1).


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  		Fig. 3.   Reflex bradycardia responses to arginine vasopressin (AVP). The graph shows regression lines relating baroreflex inhibition of HR (in beats/min) to increases in MAP (in mmHg) with AVP in sham (n = 8) or APX mice (n = 10). Values are means ± SE.

The baroreflex responses to SNP infusions are summarized in Fig. 4 and Table 1. The slope of the line for the heart rate response to SNP was the same in sham- and AP-lesioned animals.


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  		Fig. 4.   Reflex tachycardia responses to sodium nitroprusside (SNP). The graph shows regression lines relating baroreflex inhibition of HR (in beats/min) to increases in MAP (in mmHg) with SNP in sham (n = 8) or APX mice (n = 10). Values are means ± SE.

Figure 5 shows photomicrographs of the dorsal medulla at the level of the obex in representative sham-lesioned (A) and AP-lesioned mice (B). The lesion extended throughout the AP and caused minimal damage to surrounding structures.


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  		Fig. 5.   Photomicrograph of the dorsal medulla at the level of the obex in a representative sham (A) and APX mouse (B). The lesion extended throughout the area postrema and caused minimal damage to surrounding structures. CC, central canal.


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

In the present study, we evaluated the effects of AP lesion on baroreflex control of heart rate during increases in arterial pressure with PE, ANG II, and AVP or decreases in arterial pressure with SNP. We found that in conscious mice 1) ANG II-induced baroreflex inhibition of heart rate was significantly blunted relative to those observed with PE, 2) AVP-induced baroreflex inhibition of heart rate was similar to those observed with PE in both the sham and lesioned mice, 3) lesioning of the AP had no effect on the PE-induced inhibition of heart rate, and 4) lesioning of the AP facilitated ANG II-induced baroreflex control of heart rate and normalized the slope of the ANG II-induced arterial pressure-heart rate curve to that seen with PE. These results suggest that the AP is involved in the central actions of ANG II on baroreflex control of heart rate in mice.

The AP is a circumventricular organ localized in the hindbrain. Not only is the AP directly accessible to circulating peptides and hormones, it is anatomically and functionally well situated to have a direct effect on central neurons involved in cardiovascular regulation (15). The physiological evidence for the participation of the AP in central reflex function and cardiovascular control is, in part, based on the action of the circulating peptides ANG II and AVP (17, 27, 40). Both of these peptides have been shown to modulate cardiovascular function through interactions at the level of the AP. Ablation studies in rats, rabbits, and dogs have demonstrated that the central effect of ANG II on blood pressure regulation and neurogenic hypertension is dependent on the AP (3, 11, 18, 29). Additionally, an intact AP is required for ANG II to acutely modulate the arterial baroreflex control of heart rate. In this case, exogenous and endogenous ANG II shifts the baroreflex heart rate response to a higher pressure (20, 29, 30). Thus the decrease in heart rate with a given increase in pressure with ANG II is significantly less than that produced with PE. This difference is normalized after ablation of the AP. In the present study, our results confirm and extend these previous observations in conscious mice.

Like ANG II, a number of studies have also established a role for the AP in the enhancement of baroreceptor-mediated bradycardia and sympathoinhibition by systemically administered AVP. The action of circulating AVP to augment baroreflex responses was abolished by prior lesion of the AP in rabbits, dogs, and rats (1, 31, 40). A recent receptor binding study by Tribollet et al. (38) has shown the high expression of V1 receptors in the murine AP. Thus it could be speculated that AVP may have similar actions in mice. To our surprise and contrary to what might have been expected, we found that the AVP-induced baroreflex inhibition of heart rate was similar to that observed with PE in both the sham and lesioned mice. The explanation for the discrepancies seen in the mice is not readily apparent, although species differences may explain the divergent findings.

In most mammals, resting heart rates are predominantly under parasympathetic control. In mice, blockade of parasympathetic tone in general results in a minimal increase in heart rates, an indication of a low parasympathetic drive under resting conditions (13). It has also been suggested that the high resting heart rates in mice are a result of a greater sympathetic drive (26). Consequently, in the present study, the robust bradycardic responses to PE could be either due to increases in the parasympathetic drive or a withdrawl of the sympathetic drive to the heart. However, there are several studies in the literature that suggest that, in mice, vagal innervation accounts for more of the total range of heart rate changes than sympathetic innervation (19, 39). This is not unlike the autonomic regulation of heart rate in rats, except in mice the baroreflexes operate around an even higher set point. The tachycardic responses to decreases in blood pressure with SNP are considerably small (30 beats/min), an indication that, in mice, the basal heart rate is near the plateau of the cardiac baroreflex curve. However, in the absence of direct measurements of peripheral sympathetic nerve activity, it is difficult to speculate if this is due to an inability to increase sympathetic outflow or to a low chronotropic reserve. In other words, despite sufficient increases in sympathetic outflow, there is a physical limitation as to how much faster the heart can beat. In summary, the present study does not allow a definitive conclusion with regard to the role of the AP in sympathetic regulation in mice.

Clear evidence now exists for a neural pathway between the AP and the nucleus tractus solitarius (NTS) (5, 9). Activation of the AP with ANG II would result in a decrease in NTS activation by afferents, whereas activation of the AP with AVP would result in a facilitation of afferent NTS activation, which probably accounts for the ability of ANG II and AVP to regulate baroreflex sensitivity (8, 22, 33). One concern in our study was whether aspiration of AP tissue also caused damage to the subjacent NTS. Histological analysis showed that lesions were mainly restricted to the AP. Furthermore, similar values of baroreflex sensitivity for reflexly evoked tachycardia in sham-lesioned and AP-lesioned mice suggested that the AP lesion did not extensively damage baroreceptor endings in the NTS and interneuronal pathway of the baroreceptor reflex. In addition, the hypotension appears permanent up to 3 mo postlesion, which may have an influence on baroreflex sensitivity (37). Although we did not monitor the time course of blood pressure, we examined baroreflex function much longer (4 mo) after lesions were made, and resting values for blood pressure and heart rate were not different between the sham and lesioned mice. Thus this extended period may have diminished the influence of lesions on baroreflex responses to the agents tested.

In summary, in mice, ANG II-induced baroreflex inhibition of heart rate was significantly blunted relative to that observed with PE. Lesioning of the AP facilitates ANG II-induced baroreflex control of heart rate and normalized the slope of the ANG II-induced arterial pressure-heart rate curve to that seen with PE. These results suggest that the AP is involved in the central actions of ANG II on baroreflex control of heart rate in mice.


    ACKNOWLEDGEMENTS

This study was supported by National Heart, Lung, and Blood Institute Grant HL-62261.


    FOOTNOTES

Address for reprint requests and other correspondence: M. Hay, Dalton Cardiovascular Research Center, Research Park, Univ. of Missouri, Columbia, MO 65211 (E-mail: haym{at}missouri.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.

10.1152/ajpheart.00793.2002

Received 9 September 2002; accepted in final form 14 November 2002.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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11.   Cox, BF, and Bishop VS. Neural and humoral mechanisms of angiotensin-dependent hypertension. Am J Physiol Heart Circ Physiol 261: H1284-H1291, 1991[Abstract/Free Full Text].

12.   Cox, BF, Hay M, and Bishop VS. Neurons in area postrema mediate vasopressin-induced enhancement of the baroreflex. Am J Physiol Heart Circ Physiol 258: H1943-H1946, 1990[Abstract/Free Full Text].

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Am J Physiol Heart Circ Physiol 284(3):H1003-H1007
0363-6135/03 $5.00 Copyright © 2003 the American Physiological Society


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Estrogen receptor-{alpha} mediates estrogen facilitation of baroreflex heart rate responses in conscious mice
Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1063 - H1070.
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