Captopril Potentiates Chronotropic Baroreflex
Responses to Carotid Stimuli in Humans
THOMAS J. EBERT
SUMMARY Angiotensin II is a potent vasoconstrictor and has profound effects on autonomic
neural mechanisms in experimental animals. Human carotid baroreflex control of arterial pressure
and heart period was examined before and after acutely decreasing angiotensin II levels by administering 50 mg of oral captopril, an angiotensin converting enzyme inhibitor. Carotid baroreceptor
stimuli were delivered by a neck chamber worn by 14 normotensive volunteers. Four subjects received
placebo. Arterial pressure responses to carotid distent ion and tachycardia in response to carotid
compression were not changed in captopril or placebo groups; however, there was an augmented
bradycardie response to carotid stretch in captopril-treated subjects. These results indicate that
captopril has an asymmetrical effect on carotid baroreflex function and suggest that enhanced baroreflex mediated bradycardia is due to a reduction in central nervous system angiotensin II levels by
captopril, which augments vagal-cardiac responses to carotid stimuli.
(Hypertension 7: 602-606, 1985)
KEY WORDS
• angiotensin • baroreceptor
• blood pressure • carotid sinus
bits. Contrasting results were obtained from humans
with essential hypertension: heart rate and blood pressure responses to baroreceptor stimuli were unchanged
after lowering angiotensin II levels with captopril.'0
In this investigation, healthy normotensive men
were studied to determine the effects of short-term
reductions in plasma angiotensin II levels on baroreflex control of cardiac interval and blood pressure.
A NGIOTENSIN II is a potent vasoconstrictor
/ \
agent that has been shown to have an imporA. \ . tant influence on autonomic neural mechanisms. For example, intravenous infusion of pressor
doses of angiotensin attenuates baroreflex-mediated
bradycardia in sheep,1"3 rabbit/ dog,2 *"' and humans.8
However, decreasing plasma angiotensin II levels with
converting enzyme inhibitors (e.g., captopril) does not
have as consistent an effect on baroreflex function.
Several studies suggest that baroreflex sensitivity is
unchanged9 10 or decreased," while others show a potentiation1 10 12 13 of baroreflex sensitivity, after angiotensin converting enzyme inhibition.
Although the majority of these investigations have
only examined the effects of angiotensin II (or captopril) on chronotropic baroreflex responses to pressor
stimuli, several studies in experimental animals suggest that angiotensin II also attenuates sympathetic
baroreflex responses.4"7- M '5 Guo and Abboud" demonstrated that angiotensin II attenuated both the reflex
bradycardia and inhibition of lumbar sympathetic
nerve activity provoked by baroreceptor stimuli in rab-
Methods
Fourteen healthy young men, 20 to 29 years of age
(average, 24.2 yr), participated in the study after providing informed consent. The study was approved by
the institution's human research review committee.
Five subjects were instructed to follow a sodium-restricted diet (2 g/day) for 3 days before the study began. Subjects collected 24-hour urine specimens; the
collection ended with the morning void on the day of
investigation. To ensure the adequacy of collection,
these specimens were later analyzed for sodium and
creatinine content.
Subjects abstained from breakfast before arriving in
the laboratory. Radial artery cannulation was performed after Allen testing. Electrocardiogram electrodes were positioned, and subjects lay supine for 30
minutes before the studies were initiated. Control carotid baroreceptor reflex data and arterial blood samples were obtained. Ten subjects ingested 50 mg of
captopril (Squibb), and four ingested placebo. After 90
From the Department of Physiology, Medical College of Wisconsin, Milwaukee, and the Veterans Administration Hospital,
Wood, Wisconsin.
Address for reprints: Thomas J. Ebert, M.D.,Ph.D., Department
of Physiology, Medical College of Wisconsin, P.O. Box 26509,
Milwaukee, Wisconsin 53226.
Received October 13, 1984; accepted February 27, 1985.
602
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603
ANGIOTENSIN II BAROREFLEX INTERACTION IN HUMANS/£fcm
minutes baroreceptor stimuli and blood sampling were
repeated. The testing protocol was completed 2'/i
hours after ingestion of captopril or placebo. Plasma
renin activity was determined by radioimmunoassay of
angiotensin I generation.16
lyzed by least squares linear regression analysis and
Student's t tests.21 Regression slopes were compared
by analysis of covariance. Differences were considered significant at p < 0.05.
Baroreceptor Stimuli
An airtight flexible lead collar was worn by volunteers. Two types of carotid stimuli were employed: 1)
prolonged (5 sec), graded neck- suction and pressure
and 2) brief (0.4 sec), repetitive, ramped neck suction.
These stimuli were delivered in random sequence to
subjects during end-expiratory apnea. The specific
methods have been described previously.17"19 Briefly,
prolonged, graded neck suction and pressure consisted
of initially applying 10 seconds of 15 mm Hg of neck
pressure to unload carotid baroreceptors. During
breathholding, when baseline cardiac interval had stabilized, neck suction was initiated 0.8 second before
the anticipated occurrence of an atrial P wave. 20 The
RR interval immediately before the onset of neck suction was taken as the control, and the first RR interval
completed after onset of neck suction was considered
the response interval. Six intensities of neck suction
were employed ( + 1 5 to 0, - 1 0 , - 2 0 , - 3 0 , - 4 0 ,
and —50 mm Hg). The abrupt termination of each
neck suction to 15 mm Hg of neck pressure produced
graded decreases in carotid transmural pressure. These
neck pressure stimuli were also carefully timed; the
cardiac cycle occurring 4 to 5 seconds after onset of
neck suction served as the control interval for determining the triggering of neck pressure and subsequent
shortening of pulse interval. Thus, in the same breathhold, pulse interval responses to neck suction and pressure could be determined.
Results
There were no significant differences in age, height,
weight, baseline cardiac interval (1120 ± 30 vs 1107
± 21 msec), or mean blood pressure (90 ± 2 vs 92 ±
2 mm Hg) between captopril-treated and placebo
groups. Treatment with captopril resulted in a significant 4.2 mm Hg fall of mean pressure (p < 0.05)
similar to the significant 3.5 mm Hg decrease of pressure in subjects receiving placebo (p < 0.05). Neither
captopril nor placebo altered baseline cardiac interval.
There was a significant inverse relation (r =
-0.68) between 24-hour urinary sodium excretion
and the control (precaptopril) plasma renin activity.
Control plasma renin activity of 5 ± 0.07 ng/ml/hr,
increased more than threefold to 17 ± 4.2 ng/ml/hr
after angiotensin I converting enzyme inhibition. This
finding suggests formation of angiotensin II was effectively inhibited by captopril. Plasma renin activity fell
slightly in the placebo group (from 4.2 ± 2 to 3.7 ±
1.7 ng/ml/hr).
Figure 1 demonstrates the RR interval responses to
graded, prolonged neck suction. The slope of this relation is an index of carotid baroreflex sensitivity. Baroreflex slopes increased by 50% after captopril treat-
Blood pressure progressively declines during 5-second applications of neck suction. The rate of decline is
linearly related to the stimulus intensity. The mean
arterial pressure at precisely 4.0 seconds after onset of
neck suction was calculated by least squares regression
analysis. The relationship between neck suction intensity and changes in mean arterial pressure 4 seconds
after suction onset is linear and is employed in this
study as an index of carotid baroreflex control of arterial pressure.
The second type of baroreceptor stimulus was brief,
repetitive neck suction, which consisted of five consecutive electrocardiogram R-wave-triggered carotid
stimuli of increasing intensity (—10, —20, —30,
- 4 0 , - 5 0 mm Hg). Each stimulus lasted 0.4 second
and was superimposed on the natural carotid pulse. By
relating each neck suction intensity to the corresponding RR interval, baroreflex slopes are obtained in one
breathhold.18 • "
Seven duplicate trials of brief, repetitive neck suction and seven duplicate trials of each prolonged neck
suction and pressure intensity were applied to each
volunteer before and after captopril (or placebo) ingestion. Duplicate trials for each intervention were averaged for each subject. Group data represent means ±
SEM of individual averaged responses. Data were ana-
200 ,)
150 -
captopril o—-o
r-0B9
y-302x +301
p = 0001
V
100 -
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I
control «-—•
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y - 2 . 1 4 K JH S 1
p = 0001
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—•
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210
140
70
I
T
A
AS
placebo o- - - O
A
y = 5i2x 8.9
0
10
20
30
40
neck suction intensity, mmHg
50
FIGURE I. Reflex RR interval prolongation produced by
graded carotid distent ion with neck suction. Results of least
squares linear regression analysis are demonstrated. Baroreflex slopes increased significantly after captopril treatment
(p < 0.01).
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HYPERTENSION
604
VOL 7, No
4, JULY-AUGUST,
1985
0
-20
JKN
I
-40
ctptonl o—-o
captopril o-—o
r = 0.989
y = -0 09x -00
p = 0001
T
-1
r = 096
y = -1.59x-42.5
p=0001
f
-2
-60
-3 -
-80
control
r = 0.97
y = - 1 47x -47 8
-100
en -4
p - 0 001
control •— •
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& 0
1 -120
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control
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placebo o
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r=096
y= -2 9X-64 6
p = 0001
-80
-4
-110
-6
-140
-170
-200
-
placebo o--o
r = 097
y = -2 52x -72 9
p = 0001
0
10
20
30
40
neck pressure intensity, mmHg
-8
-10
50
FIGURE 2. Reflex shortening of RR interval produced by
graded carotid stimulation with neck pressure. Results of least
squares linear regression analysis are displayed. Baroreflex
slopes were unchanged by captopril and placebo treatment.
ment (p < 0.01). In contrast, baroreflex slopes were
unchanged in placebo-treated subjects. Changes in
plasma renin activity did not correlate with changes in
baroreflex slopes (r = 0.10, p > 0.05).
Figure 2 shows the RR interval responses to neck
pressure. Baroreflex slopes were not changed by either
captopril or placebo treatment. Similarly, the baroreflex-mediated decline in mean arterial pressure was not
altered by captopril or placebo treatment (Figure 3).
The responses to brief, repetitive neck suction are
shown in Figure 4. Similar to data derived from multiple applications of prolonged (5 sec) neck suction (see
Figure 1), baroreflex slopes obtained during brief stimuli in single breathholds were increased 28% after captopril treatment. Slopes were unchanged in the placebo-treated group.
Discussion
In this study, human carotid baroreflex regulation of
cardiac interval and arterial blood pressure was examined before and after inhibition of angiotensin II
formation. We found that in normotensive men, 1)
captopril administration resulted in enhanced baroreflex-mediated bradycardia but did not alter baroreflexmediated hypotension and 2) baroreflex-mediated
tachycardia in response to carotid compression was
unchanged by captopril treatment. These data suggest
0
10
20
30
40
neck suction intensity, mmHg
50
FIGURE 3. Reflex reductions of mean arterial pressure (MAP)
produced bv graded carotid distention with neck suction. Least
squares regression analysis revealed that baroreflex slopes
were unchanged bv captopril or placebo treatment.
T7777 contro*
i
E
i
) «ft«r captoprll Of placebo
HI'.'.'.'J etiango from contro<
o
w
X
a 0
"o
o
8 -2
captopril
placebo
FIGURE 4. Baroreflex slopes derived from the brief repetitive
ramped neck suction method. Similar to the prolonged method
of neck suction shown in Figure 1, slopes were significantly
increased after captopril treatment (*p < 0.05) but unchanged
in the placebo group (ns = not significant).
that angiotensin II exerts a selective influence on baroreflex responses to hypertensive stimuli: vagal responses are enhanced while sympathetic responses are
not. These conclusions are strengthened by the absence of changes in baroreflex responses after placebo
administration.
Plasma angiotensin II levels were not measured in
this study. Other reports have shown that plasma levels
are reduced 35 to 50% after short-term administration
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ANGIOTENSIN II BAROREFLEX INTERACTION IN HUMANS/Ebert
of similar doses of angiotensin converting enzyme inhibitors.1222"24 There was a wide variation in daily
sodium intake, which was achieved by placing five
subjects on a low sodium diet. Although we had hypothesized a relation between the 24-hour urinary sodium excretion or the plasma renin activity (both indirect
indices of plasma angiotensin II levels) and baroreceptor reflex responses, we found none. Furthermore,
there was no relation between the change in plasma
renin activity and the change in baroreflex response
produced by captopril. This finding does not preclude
the possibility of a direct relationship between the reductions in plasma angiotensin II levels and the enhancement of baroreflex responses.
605
A second possible explanation for captopril's effect
on baroreflex function is that baroreceptor reflexes are
reset. Hatton et al. 9 have shown that captopril treatment of sodium-depleted dogs produced a rightward
shift in the systolic pressure-RR interval relation
(change in set point) without an alteration in sensitivity. However, these effects were not evident in dogs on
normal sodium diets. In the present study blood pressure was not changed by captopril administration.
Therefore, replotting Figures 1,2, and 3 with carotid
sinus transmural pressure (systolic pressure-neck suction intensity) would not demonstrate a change in set
point.
Sympathetic Effects
Altered Carotid Baroreflex Function
Vagal Effects
These data demonstrate a highly significant augmentation of carotid to cardiac reflex gain when hypertensive stimuli (carotid distention) were applied after
angiotensin converting enzyme inhibition. This effect
was not seen during placebo or during hypotensive
stimuli (carotid compression). This differential effect
of angiotensin on vagal-cardiac responses to carotid
compression and distention also has been noted in animal studies. Guo and Abboud4 demonstrated that, during angiotensin II infusion, baroreflex inhibition of
heart rate in response to phenylephrine infusion was
attenuated while baroreflex increases in heart rate in
response to sodium nitroprusside were unchanged.
Enhanced vagal-cardiac responses to carotid stimulation may be due to 1) a direct effect of captopril, 2) a
reduction of plasma aldosterone, 3) an increase of circulating bradykinin,25 or 4) an increase of plasma prostaglandins.26 However, the most likely explanation for
augmented baroreflex function after captopril is that
plasma (and perhaps central nervous system) angiotensin II levels are decreased. This contention is supported by data from animal studies in which baroreflexmediated bradycardia was decreased by intravenous
angiotensin infusion.1-3-* Similarly, intracarotid infusion of angiotensin II has been shown to blunt baroreflex responses.7-n-28 Because angiotensin converting
enzyme inhibitors were not employed in these studies,
bradykinin and prostaglandin levels probably were unchanged.
The mechanism of this interesting interaction between angiotensin and baroreflex function is most likely due to a central effect of angiotensin that modifies
vagal-cardiac activity. Several reports have provided
data supporting this contention. Carotid sinus afferent
traffic is not altered by physiological variations in plasma angiotensin.2-4-27-29-30 Baroreflex-mediated increases in vagal efferent nerve activity are blunted by
angiotensin.2-5 Angiotensin produces a central, dosedependent reduction in vagal efferent traffic31 and has a
peripheral inhibitory action on the cardiac vagus.32 Interestingly, in the absence of baroreceptor reflexes,
angiotensin has a direct positive inotropic and chronotropic effect.15-31
In animal models, the effects of angiotensin II infusion on baroreflex control of blood pressure and sympathetic nerve activity have not been consistent. Goldstein et al.28 reported that angiotensin did not change
the reflex vasodilator response to carotid stimulation in
dogs; however, opposing findings have been reported
by others.4-6-7-33 Additionally, angiotensin infusion
may or may not alter sympathetic efferent nerve activity at rest.34"36 The reasons for these inconsistencies are
unclear. In the present study angiotensin converting
enzyme inhibition did not alter baroreflex-mediated
hypotension.
Conflicting Human Data
Mancia et al.'° applied neck suction, neck pressure,
and infused phenylephrine and sodium nitroprusside in
hypertensive patients before and after captopril ingestion. In contrast to the results of this study, they
showed that bradycardia following phenylephrine infusion was unchanged after captopril administration
while tachycardia in response to sodium nitroprusside
and hypertension in response to neck pressure were
enhanced by captopril. Several important differences
in methods should be pointed out. Mancia et al. 10 studied only hypertensive subjects. Furthermore, they applied neck chamber stimuli for 120 seconds and demonstrated an effect of captopril only on "late" (90-120
sec after stimulus onset) blood pressure responses. It is
possible that prolonged neck suction or pressure activates extracarotid reflex systems or alters cerebral
blood flow. These authors were unable to show any
effect of captopril on "early" reflex responses of blood
pressure to carotid compression or distention. These
early responses may be better indices of physiological
phenomena since neural control mechanisms in humans show moment to moment fluctuations.
Limitations
The site and mechanism of action of captopril was
not ascertained in this study, but animal studj es 7. n. 28.3i provide strong evidence that angiotensin
acts within the central nervous system to alter vagalcardiac mechanisms. The results of this study suggest
thatcaptopril-induced reductions in angiotensin II produce opposite effects. Whether potentiation of baroreflex chronotropic responses persisted during long-term
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606
HYPERTENSION
administration of captopril was not determined; only
short-term effects (within 3 hr) were examined. Blood
pressure responses to carotid compression also were
not examined.
In this study, angiotensin I converting enzyme inhibition did not alter peripheral sympathetic (hypotensive) responses to baroreflex activation and did not
influence tachycardic responses to carotid compression. However, a short-term augmentation of baroreflex-mediated bradycardia was demonstrated in normotensive men after captopril administration. This
finding is most likely due to a reduction in central
nervous system angiotensin II levels, which augments
vagal-cardiac responses to carotid stimuli. Baroreflex
potentiation of chronotropic baroreflex responses to
hypertensive stimuli by captopril may represent a contributory antihypertensive effect of this drug.
Acknowledgments
The author is grateful for the continuing support of Dr. James J.
Smith and Jill A. Barney and the secretarial assistance of Cheryl
Koch.
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Captopril potentiates chronotropic baroreflex responses to carotid stimuli in humans.
T J Ebert
Hypertension. 1985;7:602-606
doi: 10.1161/01.HYP.7.4.602
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
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