Vol. 273, Issue 4, H1713-H1718, October 1997
-Adrenoceptors in vascular capacitance responses to
unloading of carotid baroreceptors in anesthetized dogs
F.
Karim and
S. M.
Poucher
Department of Physiology, University of Leeds, Leeds LS2 9JT, United
Kingdom
 |
ABSTRACT |
The role of 
- and 
-adrenoceptors in the
total vascular capacitance responses to changing pressure in vascularly
isolated carotid sinuses of anesthetized and atropinized dogs was
investigated. A change in vascular capacitance was determined by
measuring the shift of blood in and out of a reservoir that was
connected to the aorta and maintained at a constant pressure. Changes
in carotid sinus pressure from 135 to 57 mmHg and back to 137 mmHg
resulted in a rapid vascular capacitance response of ~30 ml in the
absence of adrenoceptor antagonists. Administration of a
2-adrenoceptor antagonist
(ICI-118551) caused a significant enhancement of the capacitance
responses to similar decreases and increases in carotid sinus pressure
(~130%). Administration of a
1-adrenoceptor antagonist (CGP-20712A) did not cause any further enhancement of the responses. However, an -blocker (phentolamine) reduced the responses by 75%.
The results suggest that in the presence of a
2-adrenoceptor antagonist
vascular capacitance responses to loading and unloading of
baroreceptors are greatly enhanced and that patients suffering from
orthostatic syncope may benefit from this kind of drug.
-blocker; -blocker
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INTRODUCTION |
SEVERAL INVESTIGATIONS have clearly
demonstrated that capacitance vessels are more sensitive to changes in
sympathetic nerve activity than are resistance vessels both in the
hindlimb of anesthetized cats (23) and dogs (11, 16) and in the abdomen
of anesthetized dogs (17). It has been demonstrated that the vascular
capacitance of the abdomen, but not of the limb, plays an important
role in the baro- and chemoreceptor reflexes (6-9, 32). Reflex
responses were abolished when the sympathetic nerves to the abdominal
circulation were sectioned. Changes in the total body vascular
capacitance and mean circulatory filling pressure have also been seen
in these reflexes (15, 27, 29, 30).
There has been general agreement that capacitance vessels, particularly
those of the abdominal vascular bed, act as a potential blood reservoir
and that they can play an important role by mobilizing their contents
for circulatory homeostasis under various conditions such as changes of
posture and hemorrhage (5, 12, 14, 17, 26). Although there is
convincing evidence that -adrenergic stimulation constricts veins
and decreases vascular capacitance when baroreceptors are unloaded, the
role of -adrenergic receptors in vascular capacitance responses to
lowering of carotid sinus pressure is still unknown (1, 13, 27,
28). Shigemi et al. (28) reported in the dog a significant
reduction in the changes in the unstretched systemic vascular volume in
response to lowering of carotid sinus pressure from 200 to 50 mmHg with both an -blocker (phentolamine) and a nonselective -blocker (propranolol). It is not clear why both - and -blockers produce a
similar effect in these experiments. Several other groups also reported
similarly conflicting results (13, 24, 25).
We tested the hypothesis that
2-adrenoceptors are involved in
opposing vascular capacitance responses to changes in the activity of
carotid baroreceptors. The aim of the current experiment, therefore, was to determine the relative importance of
1- and
2-adrenoceptors in vascular
capacitance responses after loading and unloading of carotid
baroreceptors. For this we used the selective antagonists ICI-118551
(2-adrenoceptor antagonist;
Ref. 2) and CGP-20712A (1-adrenoceptor antagonist;
Ref. 22).
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METHODS |
Beagle dogs (male, 13-16 kg, n = 7; obtained from Animal Breeding Unit, Zeneca Pharmaceuticals, Alderley
Park, UK) were anesthetized by thiopental sodium (Intraval sodium, 500 mg; May and Baker), followed by chloralose (0.1 g/kg; British Drug
Houses) through a catheter placed via the right lateral saphenous vein
under local anesthesia (2% xylocaine, Astra Pharmaceuticals) so that
its tip lay in the inferior vena cava, as described previously (20). After the insertion of a cuffed tracheal tube, positive-pressure ventilation, with 40% oxygen in air, was started at a rate of 18 strokes/min and a stroke volume of ~17 ml/kg. During experiments, arterial blood gases and pH were measured (Corning 178 pH/blood gas
analyzer, Corning Scientific Instruments, Medfield, MA) frequently and
maintained within their normal limits by infusion of sodium bicarbonate
and/or by altering the setting of the respiration pump and the
flow of oxygen in inspired air.
Surgical procedure, cannulation, and hemodynamic measurements.
Aortic pressure was measured through a cannula that was passed through
the cardiac end of the left femoral artery. Right atrial pressure was
measured through a cannula inserted via the left femoral vein.
Pressures were recorded with Statham strain gauges (model P23 ID)
connected to appropriate cannulas. Both carotid sinuses were vascularly
isolated and perfused with arterial blood from the proximal end of the
left common carotid artery at a constant flow as described previously
(20). Carotid sinus pressure was regulated by altering the outflow
resistance of the carotid sinus perfusion circuit (Fig.
1). Whole body capacitance responses were measured by connecting the animal to a graduated blood reservoir via
the right common carotid (input into the reservoir) and femoral arteries (output from the reservoir; Fig. 1). To prevent stagnation of
blood in the reservoir, blood was pumped to the top of the reservoir at
a constant rate (MHRE pump, Watson Marlow) from the right common
carotid artery. The mean pressure in the abdominal aorta was controlled
by connecting it, via the right femoral artery, to the graduated blood
reservoir maintained at a constant pressure by means of a Starling
resistance and compressed air (see Fig. 1 and Ref. 15 for details). An
electromagnetic flow probe (Gould Statham cannulating type, ID 4 mm)
was placed in the circuit between the reservoir and the femoral artery.
A decrease in whole body vascular capacitance was measured as both an
increase in the volume of blood in the reservoir (3) and a change in
the signal from the flow probe. The flowmeter (model SP2202, Gould
Statham) was calibrated at the end of the experiment using the dog's
own blood.
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Fig. 1.
Schematic diagram of experimental preparation. Vascularly isolated
carotid sinus (CS) regions were perfused at constant pressure and flow
with arterial blood from right common carotid artery. Blood was pumped
through damping chamber and heat exchanger
(HE1) using roller pump
(P1). Carotid sinus pressure
(CSP) was recorded by strain gauge
(SG1) and set at desired level
by regulating outflow resistance using screw clamp (SC); blood from
sinuses was returned to left external jugular vein. Aortic pressure was
recorded by strain gauge (SG2)
attached to cannula placed in abdominal aorta via left femoral artery.
Aortic pressure was controlled by using Starling resistance and
compressed air system (air chamber, AC), which was connected to
arterial reservoir. Blood was pumped from left common carotid artery
using roller pump (P2) into
reservoir, which was primed with 30 ml dextran-saline, and returned to
animal via heat exchanger (HE2)
and cannula connected to right femoral artery. Desired pressure was
initially set in system by pressure bottle (PB) connected to mercury
manometer (MM). When aortic pressure exceeded set level, flow of air
through Starling resistance and outflow tube (OT), which was placed in
water, was enhanced and thus pressure in control system returned to
initial level. Blood flowed at constant pressure from arterial
reservoir into animal via cannulating electromagnetic flow probe and
cannula in femoral artery. CB, carotid body.
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Before connecting the perfusion circuits to the animals, we gave
heparin (185 U/kg iv) followed by a continuous infusion into the
carotid circuit at ~1
U · kg
1 · min1.
Perfusion circuits were primed with 40-50 ml of 50% dextran-50% isotonic saline [Dextraven 150, Fisons Pharmaceuticals; NaCl
solution 0.9% (wt/vol), Travenol] before they were connected to
the animals.
Experimental protocol.
Three series of experiments were performed. All animals were given
atropine sulfate (0.4 mg/kg iv) to prevent chronotropic effects of
altered baroreceptor output and to minimize the contribution from
cardiopulmonary stretch receptors. In the first series
(n = 7), effects on vascular
capacitance of lowering the pressure in the vascularly isolated carotid
sinuses from ~140 to ~50 mmHg were determined before the carotid
sinus pressure was raised to 140 mmHg. In the second series, this
protocol was repeated in five of these animals in the presence of the
2-adrenoceptor blocker (ICI-118551, 0.2 mg/kg iv over 5 min), followed by the
1-adrenoceptor blocker
(CGP-20712A, 0.2 mg/kg iv over 5 min), followed by the -adrenoceptor
blocker phentolamine (Rotinone, 1-2 mg/kg iv over 5 min). In the
third series, in two animals, the carotid sinus pressure was altered
before and after administration of CGP-20712A alone. In three of the
animals, the capacitance responses after inhibition of nitric oxide
synthase using NG-nitro-L-arginine
methyl ester (L-NAME; 50 mg/kg iv) and administration of adenosine (50- 150 mg/kg
iv), vasopressin (30 IU iv), and sodium nitroprusside (100 µg/kg iv)
were also investigated. In all cases, carotid sinus
pressure was maintained for 6 min.
Statistical analysis.
All results are expressed as means ± SE. Statistical analysis was
performed by two-factor analysis of variance. When a significant F value was found
(P < 0.05), Student's
t-test for paired data was used to
locate differences; statistical significance was deemed if
P < 0.05. Corrections for multiple
comparisons such as Bonferroni, Tukey, and Scheffé were not used
in the current study because these methods of multicomparison analysis
were designed to take into account between-group variation when each
treatment group is from separate animals. The current study used the
same animal for all drug treatments, thereby reducing variation due to
use of different animals.
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RESULTS |
Efficacy and selectivity of -adrenergic antagonists.
In pilot studies, the efficacy and selectivity of ICI-118551 (2 mg/kg)
and CGP-20712A (2 mg/kg) in anesthetized dogs was determined by the
relative inhibition of isoproterenol (1 µg/kg iv)-induced tachycardia
(1) and hindlimb
vasodilatation (2; Ref. 10). Isoproterenol produced an increase in heart rate of 108 ± 9 min1 and a decrease in
perfusion pressure of 57 ± 3 mmHg in the constant flow-perfused
hindlimb before -adrenoceptor antagonist treatment. In animals
treated with ICI-118551, the responses to isoproterenol were 108 ± 8 min1 and 27 ± 3 mmHg
for heart rate and hindlimb perfusion pressure, respectively
(n = 2). In animals treated with
CGP-20712A, the responses to isoproterenol were 8 ± 4 beats/min and
58 ± 4 mmHg for heart rate and hindlimb perfusion pressure,
respectively (n = 5).
Arterial pH and blood gases.
Throughout the experiment arterial pH,
PCO2, and
PO2 were maintained at 7.38 ± 0.01, 40.6 ± 1.4 mmHg and 106 ± 1.4 mmHg, respectively. The
hematocrit and esophageal temperature were 38 ± 1.1% and 36.9 ± 0.2°C, respectively.
Responses to changes in carotid sinus pressure.
Alteration of carotid sinus pressure resulted in a rapid change in
whole body total vascular capacitance in the absence of changes in mean
arterial blood pressure, right atrial blood pressure, and heart rate in
the animals treated with atropine alone (Fig. 2). Lowering of carotid sinus pressure from
135 ± 4 to 57 ± 3 mmHg followed by a return to 137 ± 6 mmHg
resulted in whole body vascular capacitance responses of 28.5 ± 5.3 and 29.9 ± 4.1 ml, respectively (n = 5), in the absence of hemodynamic changes (Figs. 3 and 4).
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Fig. 2.
Response to large step decrease in CSP in dog weighing 14 kg. Blood was
collected from left common carotid artery using roller pump into
arterial reservoir held at constant pressure and returned (Inflow) into
animal from reservoir via right femoral artery. Decreasing CSP caused
expulsion of 38 ml of blood from animal into reservoir before blockade
of 2-adrenoceptors
(left) and 49 ml after injection of
ICI-118551 (2-adrenoceptor
blocker, right). Large change in
systemic arterial pressure was prevented by pressure-control system
(see Fig. 1). Note that unloading of carotid baroreceptors caused
expulsion (reduction of vascular capacitance) of greater amount of
blood after blockade of
2-adrenoceptors.
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Fig. 3.
Mean arterial blood pressure (MABP), mean right atrial pressure (MRAP),
and heart rate during changes in CSP from 140 (H1) to 50 (L) to 140 (H2) mmHg in presence of atropine alone (0.4 mg/kg iv;  ); atropine + ICI-118551 (0.2 mg/kg iv;  ); atropine + ICI-118551 + CGP-20712A (0.2 mg/kg iv;  ); and atropine + ICI-118551 + CGP-20712A + phentolamine
(1-2 mg/kg iv;  ). Each point is mean ± SE
(n = 5). Statistical analysis by
Student's t-test for paired data:
a P < 0.05 vs.
CGP; b P < 0.01 vs. ICI; c P < 0.01 vs. control;
d P < 0.01 vs.
CGP.
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Fig. 4.
Blood volume response to alteration of CSP from 142 ± 3 (H1) to 52 ± 3 mmHg (L) and then returning to 148 ± 3 mmHg (H2) in
presence of atropine alone (0.4 mg/kg iv; open bars); atropine + ICI118551 (0.2 mg/kg iv; crosshatched bars); atropine + ICI-118551 + CGP-20712A (0.2 mg/kg iv; hatched bars); and
atropine + ICI-118551 + CGP-20712A + phentolamine (1-2
mg/kg iv; solid bars). Each point is mean ± SE
(n = 5). Statistical analysis by
Student's t-test for paired data:
a P < 0.05, b P < 0.02 vs.
atropine alone.
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Effect of adrenoceptor antagonist on capacitance responses.
Treatment of the animals with ICI-118551 did not affect mean arterial
blood pressure but caused a small, although statistically significant,
reduction in heart rate (7 ± 1%,
P < 0.01; Fig. 3). Subsequent
lowering of carotid sinus pressure from 147 ± 4 to 54 ± 5 mmHg
followed by a return to 154 ± 5 mmHg resulted in whole body
vascular capacitance responses of 68.1 ± 14.8 and 75.2 ± 16.2 ml, respectively (n = 5), in the
absence of hemodynamic changes (Figs. 3 and 4). The mean increase in
capacitance response to both changes in carotid sinus pressure after
ICI-118551 was 42.4 ml (95% confidence interval: 11.4-73.4 ml).
This represents a potentiation of the response by ~2.5-fold after the
inhibition of 2-adrenoceptors
(P < 0.05).
Although administration of CGP-20712A resulted in significant
reductions in mean arterial blood pressure and heart rate and an
increase in mean right atrial pressure, these were maintained constant
during the remaining protocol (Fig. 3). However, changing carotid sinus
pressure had no further effect on whole body capacitance responses
(Fig. 4). The mean difference in capacitance response to changes in
carotid sinus pressure between administration of ICI-118551 and
CGP-20712A was 10.8 ml (95% confidence interval: 
15.3 to +36.9
ml). In addition, CGP-20712A was administered before ICI-118551 in two
dogs. In these animals, the initial capacitance responses were 30.0 and
60.0 ml before antagonists. CGP-20712A resulted in either no increase
or a small increase (1.5 ml) in the vascular capacitance response.
After ICI-118551, the vascular capacitance response was increased by
55% in both animals.
Phentolamine produced a further reduction in both mean arterial blood
pressure and heart rate (14 ± 6.5 and 9 ± 2%, respectively, P < 0.05; Fig. 3). The magnitude of
the whole body capacitance response to carotid sinus pressure
alteration was reduced to ~8 ml, which represents 28% of the
response observed before administration of -adrenoceptor antagonist
(Figs. 2 and 4). The mean difference in capacitance response to changes
in carotid sinus pressure between administration of phentolamine and
control was 21.6 ml (95% confidence interval: 9.8-33.5 ml).
To determine whether the lack of a capacitance response after
phentolamine was due to general deterioration of the preparation, the
capacitance responses to adenosine, vasopressin and
L-NAME were investigated. After
administration of adrenergic blockers, the above vasoactive agents were
able to both increase and decrease the whole body vascular capacity
(Table 1).
| |
DISCUSSION |
The present investigation has clearly demonstrated that the responses
of the total vascular capacitance to loading and unloading of carotid
baroreceptors can be greatly enhanced by administration of a
2-adrenoceptor antagonist and
greatly reduced by administration of an -adrenoceptor blocker (Figs.
2 and 4). Additionally, antagonism of the
1-adrenoceptor with CGP-20712A
either alone or in combination with ICI-118551 did not further enhance
the capacitance response.
Lowering intracarotid sinus pressure always resulted in a shift of part
of the blood volume of the animal into a graduated extracorporeal
reservoir that was held at a constant pressure. Conversely, raising the
carotid sinus pressure resulted in an equivalent shift of blood back to
the animal (see Figs. 2 and 4). Blood was circulated through the
reservoir at a constant flow and at a constant pressure to keep the
systemic arterial pressure constant, and the right atrial pressure did
not change. Under this condition, a shift of blood in and out of the
reservoir must have been caused by changes in the total blood volume
from different vascular beds including the spleen. The present study
was not designed to determine the specific organ involvement. Because a
large proportion of this volume shift occurred within 1 min of changes
in carotid sinus pressure, a considerable part of this volume shift was
most likely caused by a change in the total vascular capacitance from
reflexly induced active vasoconstriction or vasodilatation (see Fig.
2). Passive elastic recoil or distension of the venous wall and fluid
absorption or filtration at the capillary bed (4, 23) were unlikely to
make any significant contribution. The hematocrit level did not change
significantly, indicating that fluid shift at the capillaries was not
significant during the determination of the capacitance responses (see
Arterial pH and blood
gases).
The shift of blood volume into the rigid extracorporeal reservoir in
response to changes in carotid sinus pressure in the present series of
experiments was similar in direction, but somewhat smaller in
magnitude, to that reported in the dog previously (15, 29, 30). This
difference was due to the larger step changes in intrasinus pressure in
earlier experiments than in the present series. Although the
experiments were not designed to identify the sources of the volume
shift, it was likely that much of this blood was shifted from the
abdominal capacitance vessels via the central circulation to the
arterial side and then to the reservoir (6, 29). However, whether the
abdominal vascular bed is the main source of blood cannot be determined
without subjecting the animal to extensive traumatic surgery as used
previously (6).
Atropine was given to prevent the chronotropic effect and to minimize
the potential contribution of cardiopulmonary and aortic receptors. It
is possible that vagal afferent fibers exert an inhibitory effect on
sympathetic efferent nerve activity that, when intact, could reduce the
capacitance response to unloading the carotid baroreceptors. Indeed, we
have shown that the vagal afferent fibers induce an inhibitory effect
on sympathetic efferent nerve activity to the kidney (21). However, we
have found that localized stimulation of the left atrial receptors does
not produce a change in total body vascular capacitance, whereas
changes in carotid sinus pressure do (19). Additionally, left atrial
receptor stimulation does not alter splenic or lumbar sympathetic
efferent nerve activity, whereas cardiac sympathetic nerve activity
increased and renal nerve activity decreased (18).
The results of the present investigation strongly suggest that the
vascular capacitance responses to unloading of the carotid baroreceptors were mediated via the -adrenergic receptors, the action of which could be enhanced when the vasodilator effect of
2-adrenoceptors was removed by
ICI-118551. The effects were not potentiated further after subsequent
administration of the 1-adrenoceptor antagonist
CGP-20712A. These results are consistent with those obtained from
anesthetized pigs, in which bilateral carotid occlusion produced a
similar capacitance response that was enhanced by -adrenoceptor
blockade with atenolol and almost completely abolished by
-adrenoceptor blockade (14). However, our results for the effects of
-adrenoceptor blockade are not consistent with those of Shigemi et
al. (28), who observed a 35% reduction in capacitance response to
lowering of intrasinus pressure after administration of propranolol. It
is not clear why removal of -adrenoceptor-induced dilator effect
caused the shift of a smaller amount of blood after lowering sinus
pressure or unloading of baroreceptors.
In conclusion, the results of these experiments may explain why
patients suffering from orthostatic syncope benefit from nonselective -blocker therapy (31). The -adrenoceptor-induced constriction of
capacitance elements after a change in position of the
-adrenergic-blocked patient from lying to standing can occur
unopposed by -adrenoreceptors. Thus a greater amount of blood would
be mobilized toward the heart to maintain an adequate cardiac filling
and output for blood pressure and cerebral perfusion.
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ACKNOWLEDGEMENTS |
The authors thank Dr. Brian Middleton of the Safety of Medicines
Department, Zeneca Pharmaceuticals, for expert advice on the
statistical analysis of the data.
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FOOTNOTES |
Address for reprint requests: S. M. Poucher, Cardiovascular and
Musculoskeletal Research Dept., Zeneca Pharmaceuticals, Mereside,
Alderley Park, Macclesfield, Cheshire SK10 4TG, UK.
Received 28 February 1997; accepted in final form 24 June 1997.
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AJP Heart Circ Physiol 273(4):H1713-H1718
0363-6135/97 $5.00
Copyright © 1997 the American Physiological Society
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Abstract
Introduction
