I.V. infusion of chloralose (0·5-1·0 mg kg-1 min-1). The depth of anaesthesia was assessed from the stability of blood pressure and heart rate, the absence of a withdrawl response to toe pinch and only a very small reflex movement to auditory stimulation.
The trachea was cannulated and the dog was artificially ventilated with O2-enriched air using a Starling 'Ideal' pump. Ventilation was adjusted to maintain normal arterial blood PO2 and PCO2 values. Molar sodium bicarbonate was infused as required to maintain normal pH values. The carotid sinuses were vascularly isolated by ligating all branches from the bifurcation except the lingual artery, whilst leaving innervation intact. An incision was made in the left side of the chest between the 4th and 5th ribs and these ribs and the sternum were divided and retracted. When the pleura was opened an end-expiratory resistance was applied equivalent to 3 cmH2O. The descending aorta was mobilized by tying and dividing the upper six pairs of intercostal arteries. The left subclavian artery was exposed, and a snare was placed around the origin of the brachiocephalic artery. The pericardium was opened and another snare was passed around the aorta just distal to the origin of the coronary arteries.
Prior to cannulation the animal was given heparin (500 i.u. kg-1), and then the perfusion circuit (Fig. 1), which was partly filled with a 2 l mixture of equal parts of mammalian Ringer solution and Dextran (Sigma) in dextrose solution, was connected to the animal in the following sequence. The medial end of the left subclavian artery was cannulated and connected to the left femoral artery, acting as a temporary arterial blood bypass to maintain perfusion of the caudal circulation during cannulations of the aorta. This bypass was clamped after the aortic cannulation. A curved stainless-steel cannula was inserted into the aortic arch to convey blood into the pressurized main reservoir from which it was distributed to the various parts of the perfusion circuit. The descending aorta was cannulated and the subdiaphragmatic circulation was pump perfused at constant flow (603U pump, Watson-Marlow, Falmouth, UK). A cannula (7 mm i.d.) was inserted into the left atrium through its appendage. Blood was drained from here into an open reservoir, from which it was pumped into the main reservoir. This controlled left ventricular filling by creating a partial left-heart bypass.
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Figure 1. Experimental preparation
A large cannula inserted into the aortic arch, with the aorta tied onto it just distal to the coronary ostea and distal to the left subclavian artery, allows control of aortic root pressure and creates a pouch outside the cannula containing aortic baroreceptors. Blood is drained from the left atria into reservoir D. Blood from this reservoir is pumped to the main reservoir, A. Blood from A is pumped into pressurized reservoirs B and C to maintain constant levels of blood in these reservoirs which supply the carotid sinuses and the aortic arch. Carotid and aortic arch blood is drained from catheters in the lingual arteries and in the brachiocephalic artery (passed down the right common carotid artery). Blood from reservoir A was pumped into the descending aorta, isolated hindlimb and cephalic circulation at constant flow. Abbreviations: CP, constant pressure; SG, strain gauge transducer; P, pump.
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The carotid sinuses were perfused with blood from a pressurized reservoir via cannulated common carotid arteries and drained via cannulated lingual arteries into the open reservoir. The cephalic circulation was perfused at constant flow (603U pump) from cannulae inserted into the peripheral end of the left subclavian artery and the central end of the left common carotid artery. A pouch of the aortic arch was created by snaring the ascending aorta onto the steel cannula and another cannula connected to a pressurized reservoir inserted into the central end of the left subclavian artery perfused the aortic pouch with blood. The pouch was drained into the open reservoir through a cannula passed down the central end of the right common carotid artery, which was tied in place close to the origin of the brachiocephalic artery. The pressure applied to the main reservoir determined aortic root pressure and hence coronary perfusion pressure.
In some experiments the left hindlimb was vascularly isolated and perfused as previously described (505U pump, Watson-Marlow) (Hainsworth et al. 1975). Briefly, the femoral artery and vein were exposed, and branches were tied and divided. Three nylon cords were placed around the muscle groups at the proximal end of the limb, taking care not to include the femoral vessels and both femoral and sciatic nerves. The femoral artery was cannulated and the limb perfused at constant flow. Isolation was achieved after connection of the circuit by tightening the snares with metal cranking devices.
The temperature of the animal was recorded by a thermistor probe in the oesophagus and was maintained at 37-39°C by a heat exchanger incorporated into the circuit and by heaters under the animal table.
Blood pressures were recorded using saline-filled nylon catheters attached to strain gauges (Gould-Statham P23 Gb) attached to nylon catheters, connected to the following: left subclavian cannula (aortic pouch pressure), lumen of the aortic cannula (coronary perfusion pressure), right carotid cannula (carotid sinus pressure), peripheral left subclavian cannula (cephalic perfusion pressure), limb perfusion cannula (limb perfusion pressure) and right femoral artery (systemic perfusion pressure, SPP). Signals were amplified (EMMA system, SE Laboratories, Feltham, UK) and recorded on VHS tape (Racal V-Store, Racal Recorders Ltd, Southampton, UK) and a direct-writing electrostatic recorder (Gould ES1000). The taped signals were subsequently digitized (100 Hz) for subsequent computer analysis (Fastdaq, Lectromed, Letchworth, UK). Before each experiment the pressure transducers were all calibrated over a range of 0-225 mmHg against a mercury column.
Experimental protocol
After connection of the perfusion circuit the pressures distending the three baroreceptor regions were held constant at 60 mmHg. About 30 min was allowed for the preparation to stabilize, during which time blood gases and pH were measured and corrected as necessary. Mean values from all eighteen dogs on pump perfusion were as follows: PO2, 178·5 ± 15 mmHg; PCO2, 40·5 ± 1·5 mmHg; pH, 7·3 ± 0·02.
Two protocols were undertaken in two groups of animals. In the first group coronary receptors were distended with a low pressure (60 mmHg) for 20 min at the end of which time a baroreflex response curve was constructed. This involved increasing the pressure distending the baroreceptor region in 30 mmHg steps of 1 min duration until no further systemic response was obtained. The coronary pressure was then raised to 180 mmHg and maintained for 20 min, after which time a further baroreflex curve was constructed. The coronary pressure was then reduced back to 60 mmHg for a further 20 min and a final baroreflex response curve was produced. In the same animals we also carried out separate tests on carotid baroreceptors using the same protocol. The order in which the carotid or coronary baroreceptor tests were performed was randomized between animals. Approximately the same length of time was left following the period of high pressure before constructing the respective baroreceptor response curves. Since the pressure applied to the coronary arteries was pulsatile due to ventricular contraction, the pressure applied to the carotid receptors was also made pulsatile with an amplitude of 38 mmHg and a frequency of 2·5 Hz (150 min-1). This was generated by a pulse generator which incorporates an electronic timer switch and two solenoid valves (Burkert timer unit 1078-2, solenoid unit 311, Bürkert Contromatic Ltd, Stroud, UK) switching between a high and a low pressure source. Adjustment of periods of high and low pressure and altering the pressures applied allows the shape of the pressure pulse to be similar to the naturally occurring pulse.
In the second group, coronary receptors were subjected to a similar conditioning regime with the high pressure being 120 mmHg and the conditioning time at low and high levels was extended to 40 min.
All response curves generated after the high pressure period were bracketed by two low pressure response curves.
During each procedure cephalic, limb and systemic blood flows were maintained constant and reflex vascular responses were determined from changes in systemic and hindlimb perfusion pressure. During each test, the pressure distending the two baroreceptor regions not under investigation was maintained constant at 60 mmHg.
These experiments were carried out in accordance with current United Kingdom legislation, the Animals (Scientific Procedures) Act 1986. Experiments were terminated by exsanguination of the animal.
Analysis of the results
Only results from tests where the overall vascular response was 23 mmHg or greater over the entire baroreceptor pressure range were analysed. The method used to analyse the results utilized a commercially available computer software package (GraphPad Prism v. 2.0, GraphPad Software Inc., San Diego, CA, USA) to fit the non-linear third order polynomial regression curve which was determined to best fit these data points (F test).
We determined from each curve the baroreceptor distending pressure which corresponded to 50 % of the overall systemic response (BP50). The baroreflex response curves were also compared by analysing the data using 2-way ANOVA. Threshold values are not reported as in many experiments large responses were obtained in response to the first pressure increase.
Each individual test was analysed by these methods, and the values presented are the averages of the tests in each animal.
All values reported are means ± S.E.M. and the statistical significance was assessed by Student's paired t test unless otherwise stated.
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RESULTS |
Coronary and carotid baroreceptor responses after conditioning at 60 and 180 mmHg
Results were obtained from six dogs in which both carotid and coronary baroreceptors were sequentially conditioned at 60, 180 and 60 mmHg for 20 min. During the test of one of the baroreceptor groups, the pressure distending the other baroreceptor regions was maintained at 60 mmHg. From the averages of the responses to changes in carotid pressure after conditioning at 60 mmHg, the overall decrease in systemic pressure was from 171·4 ± 6·8 to 93·2 ± 7·5 mmHg (-45·2 ± 5·2 %) and the BP50 was 135·3 ± 6·8 mmHg. The BP50 value obtained following the first conditioning pressure of 60 mmHg was not significantly different from the BP50 value obtained following the final conditioning pressure of 60 mmHg (BP50 = 129·9 ± 8·9 and 139·9 ± 8·0 mmHg, respectively; P = 0·4). After conditioning at 180 mmHg, increases in carotid pressure decreased systemic pressure from 199·2 ± 16·5 to 95·5 ± 6·0 mmHg (-50·6 ± 5·0 %). The BP50 significantly increased to 155·6 ± 8·3 mmHg, an increase of 20·3 ± 8·3 mmHg (P < 0·05) from the response after conditioning at the low pressure. Analysis of the data points using 2-way ANOVA confirmed a significant shift in the baroreflex response curves following conditioning at the high pressure (P < 0·0001). The resting systemic pressure levels prior to the low and high response curves were 172·1 ± 7·8 and 197·9 ± 16·4 mmHg, respectively (P = 0·08). The group responses of systemic perfusion pressure after conditioning at 60 and 180 mmHg for 20 min showing the shift in the carotid baroreceptor stimulus-response curve is shown in Fig. 2 and the mean data are summarized in Table 1.
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Figure 2
Group carotid curves fitted to a third order polynomial where the carotid baroreceptors were conditioned at 60 mmHg (----) and 180 mmHg (--) for 20 min (n = 6).
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Table 1. BP50 values for carotid and coronary baroreflex curves conditioned at 60 and 180mmHg for 20 min and coronary baroreflex curves conditioned at 60 and 120 mmHg for 40 min
| Carotid, 20 min | Coronary, 20 min | Coronary, 40 min |
| 60 mmHg | 180 mmHg | 60 mmHg | 180 mmHg | 60 mmHg | 120 mmHg |
| Systemic BP50 (mmHg) | 135·3 ± 6·8 (6) | 155·6 ± 8·3 (6) * | 94·7 ± 8·3 (6) | 91·0 ± 3·8 (6) | 111·3 ± 12·0 (6) | 106 ± 14·3 (6) |
| Limb BP50 (mmHg) | - | - | - | - | 119·5 ± 16·5 (5) | 112·8 ± 16·5 (6) |
* P < 0·05; number of animals in parentheses.
In the same dogs after conditioning the coronary baroreceptors at 60 mmHg for 20 min, increases in coronary pressure decreased systemic perfusion pressure from 158·6 ± 9·8 to 91·0 ± 8·3 mmHg (-41·5 ± 4·8 %). The BP50 value obtained following the first conditioning pressure of 60 mmHg was not significantly different from the BP50 obtained following the second conditioning pressure of 60 mmHg (BP50 = 95·9 ± 9·1 and 91·6 ± 6·9 mmHg, respectively; P = 0·8). The averaged BP50 for the low conditioning pressure (60 mmHg) was 94·4 ± 8·3 mmHg. This value was not significantly changed by conditioning the coronary receptors at 180 mmHg for 20 min (91·1 ± 3·8 mmHg; P = 0·6) and analysis of the data points using 2-way ANOVA confirmed that they were not significantly different (P = 0·9). Figure 3 shows the group responses of systemic perfusion pressure after conditioning the coronary receptors at 60 and 180 mmHg for 20 min demonstrating the absence of any shift in the stimulus-response curve. The data from all six dogs are compared with the carotid responses in Table 1. The resting systemic pressure levels prior to the low and high response curves were 159·8 ± 10·0 and 172·0 ± 15·6 mmHg, respectively (P = 0·4).
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Figure 3
Group coronary curves fitted to a third order polynomial where coronary baroreceptors had been conditioned at 60 mmHg (----) and 180 mmHg (--) for 20 min (n = 6).
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Coronary baroreceptor responses after conditioning the baroreceptors at 60 and 120 mmHg
In six dogs after the coronary arterial pressure had been maintained at 60 mmHg for 40 min a stimulus-response curve was constructed by increasing coronary pressure from 60 mmHg in steps of approximately 30 mmHg to a high level where the response saturated. This resulted in step decreases in perfusion pressure to both the systemic circulation and the perfused hindlimb (n = 5). After the baroreceptors had been conditioned by maintaining coronary pressure at 120 mmHg for 40 min, coronary pressure was reduced to 60 mmHg and once systemic and limb pressures had recovered to their former levels another stimulus-response curve was constructed. A further low stimulus-response curve was obtained again after the coronary pressure had been maintained at 60 mmHg for a further 40 min. From the averages of the responses after conditioning at 60 mmHg, systemic arterial perfusion pressure decreased from 170·0 ± 15·0 to 92·6 ± 8·7 mmHg (-42·4 ± 4·3 %) and the BP50 was 111·3 ± 12·0 mmHg. The values for BP50 obtained following the two 60 mmHg periods of conditioning pressure were not different (107·6 ± 12·6 and 113·6 ± 12·1 mmHg; P = 0·4). After conditioning for 40 min at 120 mmHg, there was no significant change in the BP50 value (106 ± 14·3 mmHg; P = 0·5) and analysis of the data points using 2-way ANOVA confirmed that they were not significantly different (P = 0·2). The BP50 calculated from the changes in hindlimb vascular resistance was also unaffected by the conditioning pressure (119·5 ± 16·5 and 112·8 ± 16·5 mmHg for the low and high curves, respectively; paired t test, P = 0·4; 2-way ANOVA, P = 0·5). The resting systemic pressure levels prior to the low and high response curves were 169·4 ± 15·0 and 209·6 ± 23·3 mmHg, respectively (P = 0·075).
Figure 4 shows group responses of systemic perfusion pressure after conditioning at 60 mmHg and 120 mmHg for 40 min. The mean responses from all dogs are listed in Table 1.
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Figure 4
Group coronary curves fitted to a third order polynomial where coronary baroreceptors had been conditioned at 60 mmHg (----) and 120 mmHg (--) for 40 min (n = 6).
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DISCUSSION |
The stimulus-response curves of two main groups of classical baroreceptors, those located in the carotid sinuses and aortic arch, have been shown to reset towards the prevailing pressure within a period of 5-20 min (Koushanpour, 1991). In those studies the acute resetting is characterized by shifts in the threshold and inflexion pressures of the baroreceptor response curve towards the conditioning pressure.
In this study we have examined whether the coronary baroreflex also resets over conditioning periods of 20 min using conditioning pressures of 60 and 180 mmHg, and 40 min using pressures of 60 and 120 mmHg. A pressure of 120 mmHg was applied for the longer conditioning period since it produced near saturation of the vascular response and was found to result in a more stable preparation. The reasons for setting the low holding pressure at the hypotensive level of 60 mmHg rather than a pressure close to the normal arterial pressure in dogs of 101·6 mmHg (Cowley et al. 1973) was to provide maximum pressure shift to assist the resetting process and because of the low threshold for the coronary baroreceptor reflex. It is evident from the plots of coronary responses in this paper and from our previously published results that the threshold for the coronary baroreceptors is extremely low (McMahon et al. 1996b) and that the first step increase in pressure generally produces a large vascular response. We were unable to examine increases in pressure from a lower starting pressure as this would cause myocardial ischaemia and be likely to confound the haemodynamic responses. For this reason it was not possible, in this study, to investigate whether the threshold of the response was shifted towards the prevailing pressure as has been described for carotid receptors (Kunze, 1981; Heesch et al. 1984; Tan et al. 1989b; Chen et al. 1993) and aortic receptors (Coleridge et al. 1981; Munch et al. 1983; Undesser et al. 1984) although we were able to determine any possible shift in the BP50. Furthermore the range of pressures that we examined did cover more than the physiological range
We determined effects of conditioning the coronary baroreceptors at 120 mmHg for 40 min and 180 mmHg for 20 min and whichever regime was used there was no difference between the curves (2-way ANOVA). Similarly there was no difference between the BP50 values of the curves obtained following the high and low pressures. This feature is unique to the coronary reflex as exposure of carotid and aortic baroreceptors to different pressures is characterized by a shift in the BP50. In the same animals using the same regime we were able significantly to increase the BP50 of the carotid response curve. This agrees with previously published results (Tan et al. 1989b; Tan & Zucker, 1989). The difference in the effects on carotid and coronary baroreceptors was not due to any procedural differences. Experiments were compared within the same animals, the same conditioning pressures were applied for the same times and the same steps of baroreceptor pressure were applied for the same durations.
In this study the coronary and carotid baroreceptors were conditioned and the curves constructed using pulsatile pressures. There is much disagreement in the literature as to whether pulsatile pressures attenuate or augment the resetting process (Tan & Zucker, 1989; Andresen & Yang, 1990). In an earlier study we showed that the coronary receptors, unlike the carotid receptors, are insensitive to changes in arterial pulse pressure (McMahon et al. 1996b). In this study the pressures distending both coronary and carotid baroreceptors were pulsatile, so the difference in the resetting characteristics could not have been due to effects of pulsatility.
These experiments have shown the coronary baroreceptors to be resistant to the acute resetting process over a physiological range of pressures. The reason for this is unknown. It is unlikely to be our chosen conditioning regime as the same regime applied to carotid receptors caused resetting. One possibility which we have not excluded would be that the coronary baroreceptors reset at extremely low pressures (i.e. below 60 mmHg), although the physiological relevance of this is unclear. Another possibility may be related to the location of the coronary baroreceptors, which have been located principally to the left coronary artery (Abráhám, 1962; Okinaka et al. 1963; Drinkhill et al. 1993). Due to the fact that they are surrounded by myocardium, the artery may expand less in response to the same pressure than either the carotid sinus or aortic arch and this may limit the mechanical change known as creep (Coleridge et al. 1981; Coleridge et al. 1984). However, this is unlikely to be the only explanation since creep has been shown not always to occur in other regions where acute resetting was exhibited (Heesch et al. 1984; Munch & Brown, 1985). Aortic receptors acutely reset even in the absence of endothelium and smooth muscle (Kunze, 1985).
A further explanation for the lack of coronary resetting could be the effect of a central mechanism. A central mechanism responsible for acute carotid baroreceptor resetting in the dog has been demonstrated, producing resetting of baroreceptors not exposed to pressure changes (Tan et al. 1989a). We have already demonstrated that coronary baroreceptors have different effects on sympathetic outflow as compared with carotid and aortic receptors and therefore must have different connections within the central nervous system (Drinkhill et al. 1996). This difference may account for the lack of coronary resetting.
When the conditioning period for coronary receptors was extended to 40 min, as previously discussed, we still did not detect a shift in the distending pressure-vascular response relationship. However, we did observe that the level to which systemic pressure recovered after the period at high pressure was greater in four out of the six animals investigated and in one animal the resting systemic pressure had increased by 102 mmHg. A similar effect was observed for the carotid response group. Though this difference did not reach significance it does suggest that other mechanisms may affect the baroreflex stimulus-response relationship when pressure is raised for longer periods. For example it is known that exposure of the adrenergic receptors to their agonist results in rapid desensitization (Liggett & Raymond, 1993). The reduced sympathetic activity which would occur during the period of high baroreceptor distending pressure would promote adrenergic resensitization and may explain our observation of higher systemic pressures.
Though the reason for the failure of resetting of coronary baroreceptors is unclear, the physiological significance is intriguing. Resetting of carotid and aortic receptors towards the prevailing pressure allows these receptors to buffer changes in pressure over a wide range but implies that these receptors are not likely to be effective at controlling mean blood pressure (Cowley et al. 1973; Scher, 1977). The position of the coronary reflex response curve is fixed, and therefore this reflex would oppose the pressure change to a greater extent than the aortic or carotid reflexes which shift their operating range over time to signal the new arterial pressure rather than opposing the pressure change. This would imply that the coronary baroreceptor reflex acts as a fixed mechanism controlling the level of arterial blood pressure. However, although this suggests that coronary baroreceptors may have a role in long-term regulation of arterial pressure, we do not yet know whether, like the carotid and aortic baroreceptors, coronary baroreceptors reset when the pressure to which they are exposed is changed for prolonged periods.
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REFERENCES |
| Abráhám, A. (1962). Die nervenversorgung der kranzgefässe des herzens. Archives Internationales de Pharmacodynamie et de Thérapie 139, 17-27. |
|
| Al-Timman, J. K. A., Drinkhill, M. J. & Hainsworth, R. (1993). Reflex responses to stimulation of mechanoreceptors in the left ventricle and coronary arteries in anaesthetized dogs. The Journal of Physiology 472, 769-783 |
[Abstract] |
| Andresen, M. C. & Yang, M. (1990). Dynamic and static conditioning pressures evoke equivalent rapid resetting in rat aortic baroreceptors. Circulation Research 67, 303-311 |
[Abstract] |
| Brunner, M. J. & Kligman, M. D. (1992). Rapid resetting of baroreflexes in hypertensive dogs. American Journal of Physiology 262, H1508-1514 |
[Medline] |
| Chen, H. I., Chang, K.-C., Liu, H.-C. & Lin, C.-H. (1993). Acute adaptation and resetting of the baroreflex control of vascular resistance in the canine hindquarters and mesentery. Pflügers Archiv 424, 276-284 |
[Medline] |
| Coleridge, H. M., Coleridge, J. C. G., Kaufman, M. P. & Dangel, A. (1981). Operational sensitivity and acute resetting of aortic baroreceptors in dogs. Circulation Research 48, 676-684 |
[Abstract] |
| Coleridge, H. M., Coleridge, J. C. G., Poore, E. R., Roberts, A. M. & Schultz, H. D. (1984). Aortic wall properties and baroreceptor behaviour at normal arterial pressure and in acute hypertensive resetting in dogs. The Journal of Physiology 350, 309-326 |
[Abstract] |
| Cowley, A. W., Liard, J. F. & Guyton, A. C. (1973). Role of the baroreceptor reflex in daily control of arterial blood pressure and other variables in dogs. Circulation Research 32, 564-576 |
[Medline] |
| Drinkhill, M. J., McMahon, N. C. & Hainsworth, R. (1996). Delayed sympathetic efferent responses to coronary baroreceptor unloading in anaesthetized dogs. The Journal of Physiology 497, 261-269 |
[Abstract] |
| Drinkhill, M. J., Moore, J. & Hainsworth, R. (1993). Afferent discharges from coronary arterial and ventricular receptors in anaesthetized dogs. The Journal of Physiology 472, 785-799 |
[Abstract] |
| Hainsworth, R., Karim, F. & Stoker, J. B. (1975). The influence of aortic baroreceptors on venous tone in the perfused hind limb of the dog. The Journal of Physiology 244, 337-351 |
[Abstract] |
| Heesch, C. M. & Carey, L. A. (1987). Acute resetting of arterial baroreflexes in hypertensive rats. American Journal of Physiology 253, H974-979 |
[Medline] |
| Heesch, C. M., Thames, M. D. & Abboud, F. M. (1984). Acute resetting of aortic baroreceptors. American Journal of Physiology 247, H824-832 |
[Medline] |
| Koushanpour, E. (1991). Baroreceptor discharge behaviour and resetting. In Baroreceptor Reflexes: Integrative Functions and Clinical Aspects, ed. Persson, P. B. & Kirchheim, H. R., pp. 9-44. Springer-Verlag, Berlin. |
|
| Kunze, D. L. (1981). Rapid resetting of the carotid baroreceptor reflex in the cat. American Journal of Physiology 241, H802-806 |
[Medline] |
| Kunze, D. L. (1985). Role of baroreceptor resetting in cardiovascular regulation: acute resetting. Federation Proceedings 44, 2408-2411 |
[Medline] |
| Liggett, S. B. & Raymond, J. R. (1993). Pharmacology and molecular biology of adrenergic receptors. Clinical Endocrinology and Metabolism 7, 279-306. |
[Medline] |
| McCubbin, J. W., Green, J. H. & Page, I. H. (1956). Baroreceptor function in chronic renal hypertension. Circulation Research 4, 205-210. |
|
| McMahon, N. C., Drinkhill, M. D. & Hainsworth, R. (1996a). Reflex vascular responses from aortic arch, carotid sinus and coronary baroreceptors in the anaesthetized dog. Experimental Physiology 81, 397-408 |
[Medline] |
| McMahon, N. C., Drinkhill, M. D. & Hainsworth, R. (1996b). Vascular responses to stimulation of carotid, aortic and coronary artery baroreceptors with pulsatile and non-pulsatile pressures in anaesthetized dogs. Experimental Physiology 81, 969-981 |
[Medline] |
| Mendelowitz, D. & Scher, A. M. (1990). Pulsatile pressure can prevent rapid baroreflex resetting. American Journal of Physiology 258, H92-100 |
[Medline] |
| Munch, P. A. (1992). Discharge characteristics and rapid resetting of autoactive aortic baroreceptors in rats. The Journal of Physiology 458, 501-517 |
[Abstract] |
| Munch, P. A., Andresen, M. C. & Brown, A. M. (1983). Rapid resetting of aortic baroreceptors in vitro. American Journal of Physiology 244, H672-680 |
[Medline] |
| Munch, P. A. & Brown, A. M. (1985). Role of vessel wall in acute resetting of aortic baroreceptors. American Journal of Physiology 248, H843-852 |
[Medline] |
| Okinaka, S., Ikedo, M., Hashiba, K., Fujii, J., Kuramoto, K., Terasawa, F., Ozawa, T., Kaneko, J. & Murata, K. (1963). Pressoreflex arising from the left coronary artery. Japanese Circulation Journal 27, 557-584. |
|
| Scher, A. M. (1977). Carotid and aortic regulation of arterial blood pressure. Circulation 56, 521-528 |
[Medline] |
| Tan, W., Panzenbeck, M. J., Hajdu, M. A. & Zucker, I. H. (1989a). A central mechanism of acute baroreflex resetting in the conscious dog. Circulation Research 65, 63-70 |
[Abstract] |
| Tan, W., Panzenbeck, M. J. & Zucker, I. H. (1989b). Acute baroreflex resetting and its control of blood pressure in an open loop model. Basic Research in Cardiology 84, 431-441 |
[Medline] |
| Tan, W. & Zucker, I. H. (1989). Acute carotid baroreflex resetting in conscious dogs. The Journal of Physiology 416, 557-569 |
[Abstract] |
| Undesser, K. P., Lynn, M. P. & Bishop, V. S. (1984). Rapid resetting of aortic nerves in conscious rabbits. American Journal of Physiology 246, H302-305 |
[Medline] |
|
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Acknowledgements
This study was supported by a Medical Research Council grant. The technical assistance of Mr D. Myers is also gratefully acknowledged.
Corresponding author
N. McMahon: Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK.
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S. Ogoh, R. M. Brothers, Q. Barnes, W. L. Eubank, M. N. Hawkins, S. Purkayastha, A. O-Yurvati, and P. B. Raven
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Top
Introduction
-chloralose (100 mg kg-1; Vickers Laboratories Ltd, Pudsey, UK) dissolved in 0·9 % saline solution. Anaesthesia was maintained by a continuous 
