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(Hypertension. 1997;30:848-853.)
© 1997 American Heart Association, Inc.
Articles |
Moderately Obese, Insulin-Resistant Women Exhibit Abnormal Vascular Reactivity to Stress
From the Department of Medicine, State University of New York, and Millard Fillmore Health System, Buffalo, NY.
Correspondence to Bong Hee Sung, PhD, Department of Medicine, Millard Fillmore Hospital, 3 Gates Circle, Buffalo, NY 14209. E-mail bsung{at}mfhs.edu
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Abstract |
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Abstract To define the hemodynamic implications of insulin resistance (IR), we compared 10 normotensive, insulin-resistant women who had abnormal glucose tolerance tests with 10 age-matched healthy normotensive women with normal glucose tolerance tests with respect to mental arithmetic and handgrip responses. Hemodynamic variables obtained at baseline and during stress included heart rate, blood pressure, cardiac output, and systemic vascular resistance. The IR group weighed more (84 versus 66 kg). Screening BP was similar (123/72 versus 120/68 mm Hg, P=NS) between groups although baseline diastolic BP at testing day was higher in the IR group than control group (75 versus 65 mm Hg, P<.05). The IR group showed a significantly greater increase in systolic (18% versus 10%, P<.01) and diastolic (24% versus 12%, P<.01) blood pressure responses to mental stress than the control group. During mental stress, the control group demonstrated increased cardiac output (1.4 L/min) and decreased systemic vascular resistance (-120 dyne · s · cm-5), whereas IR subjects demonstrated increased systemic vascular resistance (119 dyne · s · cm-5; group difference, P<.02) with only a small increase in cardiac output (0.5 L/min). Handgrip also caused a greater increase in systemic vascular resistance in the IR group (252 versus 64 dyne · s · cm-5, P<.05), with a correspondingly greater increase in blood pressure than control subjects. Baseline blood pressure was correlated with weight (r=.41, P<.02) and stress blood pressure with fasting insulin (r=.51, P<.001) and glucose-to-insulin ratio (r=-.55, P<.001). We conclude that insulin resistance is associated with an exaggerated blood pressure response to stress; an enhanced vasoconstriction to stress may mediate this response. This hyperreactivity may be a marker for future hypertension in obese, normotensive, hyperinsulinemic individuals.
Key Words: insulin resistance • vascular resistance • blood pressure • stress
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Introduction |
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Clustering of risk factors such as glucose intolerance, hypertension, obesity, and dyslipidemia are well established, and insulin resistance has been implied to mediate this association.1 2 3 4 5 6 Although increased sodium absorption and sympathetic stimulation have been reported with hyperinsulinemia, thus linking them to hypertension, experimental data from animal and human studies suggest that insulin has vasodilator properties.7 8 9 10 Despite the clear demonstration of insulin resistance associated with hypertension, the underlying mechanisms remain elusive.
Mental arousal and physical exertion are important sources of the physiological variation in blood flow. Individual differences in the hemodynamic response pattern to a psychological or physical stimulus have been implicated to be associated with disease outcome. Enhanced blood pressure (BP) response to stress has been reported to be a predictor for the future development of hypertension.11 12 13 14 Although insulin resistance is positively associated with hypertension, the relationship between insulin resistance and BP response to stress is currently unknown. Thus, investigation of whether insulin resistance influences the hemodynamic response to physiological modulators of vascular tone is of considerable importance.
Cardiovascular risk factors are highly prevalent in U.S. women. Studies show that 51% of white women and 79% of black women older than 45 years of age have hypertension.15 16 After 45 years of age, women are twice as likely as men to develop diabetes mellitus, and studies suggest that diabetes eliminates protection against coronary heart disease in premenopausal women.17 Thus, there is a particular need for paying attention to women who are at high risk. In this study, we examined the BP response to a mental arithmetic test (MAT) and handgrip test in healthy, normotensive, insulin-resistant women to identify early changes associated with insulin resistance and BP regulation.
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Methods |
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Study Population
Healthy, normotensive women were recruited through advertisements in the local community. Respondents were initially interviewed by telephone, and those who met the inclusion criteria underwent physical examination and BP screening. Study subjects did not have clinical or laboratory evidence of diabetes mellitus, hypercholesterolemia, or hypertension and were not taking any medication. Smokers were excluded from the study. The final study group consisted of 20 healthy, normotensive women (mean age, 42±11 years). The study was approved by the Institutional Review Board of the Millard Fillmore Hospital.
BP Screening Session
During the BP screening session, the subject sat quietly in a
neutral office environment for 5 minutes. Afterward, a nurse attached
an automated BP monitor (Colin Press-Mate, Colin Medical Instruments
Corp), and five readings were obtained at 2-minute intervals. A normal
BP (<140/90 mm Hg) from the screening was required for further
testing.
Oral Glucose Tolerance Test
An oral glucose tolerance test (GTT) was performed after women
had fasted 12 hours to determine insulin resistance. After a fasting
blood sample was drawn, a 75-g oral glucose load was administered.
Blood samples were obtained 30, 60, 90, and 120 minutes thereafter for
determination of glucose and insulin levels.
Hemodynamic measurements were made 30, 60, 90, and 120
minutes to examine the effects of acute glucose loading on systemic
hemodynamics. Serum insulin level was measured by
radioimmunoassay. The fasting glucose-to-insulin ratio was calculated
as an index of insulin resistance.18
Study Protocol
The subjects reported to the laboratory at 8 am after 12 hours
of fasting. All study subjects were requested to refrain from alcohol
and caffeine at least 12 hours before the experiment. Subjects were
equipped with electrocardiographic electrodes, an automated BP monitor
(Colin Press-Mate), and an impedance cardiograph (RTI Bioimpedance
Monitor). The protocol consisted of a 20-minute baseline, a 5-minute
MAT, and a 3-minute handgrip test. There was a 10-minute recovery
period between the MAT and handgrip test and after the handgrip
test.
Mental Arithmetic Test
After subjects rested in a comfortable chair for 20 minutes,
baseline hemodynamic measurements were made.
Participants were instructed to serially subtract threes and sevens
from a three-digit number during 5-minute periods. They were asked to
make a subtraction out loud and provide answers as quickly and
accurately as possible. When an incorrect answer was given, they were
asked to repeat the subtraction. Hemodynamic
measurements were initiated 1 minute after the onset of the task and
recorded at 1-minute intervals during 5 minutes of serial
subtraction and the recovery period.
Handgrip Test
After 10 minutes of recovery from the serial subtraction,
prehandgrip baseline hemodynamic measurements were
recorded, and maximal handgrip was determined. Subjects held one
third of maximal grip load for 3 minutes.
Cardiovascular measurements were made at baseline,
1-minute intervals during handgrip, and during recovery.
Hemodynamic Measurements
Cardiovascular variables consisting of heart
rate, BP, stroke volume, cardiac output, and calculated systemic
vascular resistance were measured. Stroke volume and cardiac output
were measured by impedance cardiography from ensemble-averaged
waveforms. Impedance cardiography permits repetitive determinations of
such parameters in response to mental and physical stress
under different stimulus conditions. The technique and data documenting
its reliability and validity have been previously
described.19
Statistical Analysis
Values are expressed as mean±SD. A multiple regression
analysis with forward and backward stepping with interaction
was performed to identify factors that influence BP at baseline and
during stress of the study group. Next, two-way ANOVA or ANCOVA with
repeated measures was performed to examine interaction between stress
effect and group difference. Systat (Systat Inc, Evanston, IL) was
used. A value of P<.05 was considered significant.
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Results |
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Predictors of BP at Rest and During Stress
Table 1
shows characteristics of the study group. The study
population was all women between the ages of 24 and 61 years. Screening
BP values were 102 to 135 mm Hg for systolic BP and 52 to
82 mm Hg for diastolic BP. Our study group had wide
ranges of body weight (51 to 107 kg), body mass index (22 to 42
kg/m2), and fasting glucose (73 to 121 mg/dL)
and fasting insulin (5.0 to 25.9 µU/mL) levels. A multiple regression
analysis showed that body weight was significantly associated
with baseline diastolic BP (r=.405,
P=.02) but not with other hemodynamic
variables. Body weight was also significantly correlated with
fasting insulin level (r=.594, F=9.801, P=.006)
and glucose level (r=.527, F=5.759, P=.03).
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Serial subtraction is considered to be a moderately challenging
cognitive stressor and has been used as a standard mental stress test.
MAT increased systolic BP into the hypertensive range
(>140 mm Hg) in 50% of study subjects. Six of 20 (30%)
subjects also had diastolic BP greater than 90 mm Hg
during MAT. We performed a multiple regression analysis which
considers all variables simultaneously to detect
significant factors influencing BP during mental stress. Table 2 summarizes the results of multiple
regression analysis. Fasting insulin level and the
glucose-to-insulin ratio, which indicates insulin sensitivity, were
significant predictors of the BP response to stress independent of age,
body weight, and baseline BP. Fig 1A
illustrates the relationship between fasting insulin levels and mean BP
(r=.51, P<.001) response to MAT, and Fig 1B
illustrates the significant inverse relationship between the
glucose-to-insulin ratio and mean BP (r=-.55,
P<.001) response to mental arithmetic.
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Group Classification
To examine the role of insulin resistance on the
hemodynamic response to stress, we made a distinction
between an insulin-resistant (IR) group and normal control
group on the basis of the results of the GTT. Ten subjects had normal
GTT and 10 had abnormal GTT. The abnormal GTT group had significantly
lower glucose-to-insulin ratios than the normal GTT group (6±1.6
versus 11±3.4, P<.01), confirming reduced insulin
sensitivity. Both groups were comparable in age and height, but the IR
group had significantly higher body weight and body mass index than the
control group (both P<.001). Although screening BP values
were comparable between the IR and control groups (123/72 versus
120/68 mm Hg, P=NS), baseline diastolic BP
values at the test session were significantly higher in the IR group
than control group (75 versus 65 mm Hg, P<.05). Heart
rate, systolic BP, cardiac output, and systemic vascular
resistance were not significantly different between the groups.
Comparison of Hemodynamic Response Between IR and
Control Groups
There was no significant difference between pre-MAT baseline and
10 minutes after MAT (pre-handgrip baseline) in any of the measured
hemodynamic variables. Thus, we averaged both and
used these averages as baseline values for the MAT and handgrip test.
The IR group had a significantly higher systolic BP (18%
versus 10%, P<.01) and diastolic BP (24%
versus 12%, P<.01) response during MAT than the control
group. MAT increased systolic BP into the hypertensive range
(>140 mm Hg) in 9 of 10 (90%) subjects in the IR group compared
with 1 of 10 (10%) subjects in control group. Five of 10 (50%)
subjects in the IR group also had diastolic BP greater than
90 mm Hg, compared with none in the control group. Therefore,
mean increments in systolic and diastolic BPs
during MAT were significantly higher in the IR group than the control
group (group-by-stress interaction, P<.02).
Handgrip also caused an increase in heart rate and BP for both groups.
The IR group had a greater increase in diastolic BP (21
versus 13 mm Hg) and vascular resistance (250 versus 65 dyne
· s · cm-5, P<.01) than
the control group. In contrast, the control group had a greater
increase in heart rate (17 versus 12 beats per minute; stress-by-group
interaction, P<.05) and cardiac output (0.85 versus 0.4
L/min, P=.03) than the IR group. Thus, the IR group showed a
pattern of limited flow and enhanced vascular resistance during stress.
Handgrip test also increased systolic BP into hypertensive
ranges in all subjects of the IR group and 6 of 10 control subjects.
Eight members of the IR group (80%), compared with 2 of the control
group (20%), had diastolic BP greater than 90 mm Hg
during the handgrip test. Table 3
summarizes baseline hemodynamics and
hemodynamic responses to MAT and handgrip.
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Next, we examined the underlying mechanism of increased BP during MAT
and the handgrip test. Fig 2 compares
changes in cardiac out put and systemic vascular resistance during
mental and physical stress between the IR and control groups. The
control group raised BP by increasing cardiac output (1.4 L/min) and
decreasing systemic vascular resistance (-120 dyne · s ·
cm-5). In contrast, there was a significant
increase in vascular resistance and insignificant increase in cardiac
output during mental stress in the IR group. This paradoxical increase
in vascular resistance response to mental stress caused an enhanced BP
response during MAT. Handgrip also caused a greater increase in
systemic vascular resistance in the IR group (252 versus 64 dyne
· s · cm-5, P<.05), with
a correspondingly greater increase in BP than in control subjects.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Mental arousal and physical exertion are two common physiological stressors that can elicit different hemodynamic response patterns. In contrast to handgrip and cold pressor tests, MAT has been known to increase forearm blood flow and decrease systemic vascular resistance.20 Our insulin-resistant group showed a paradoxical systemic vascular resistance response to MAT and enhanced vascular resistance to the handgrip test. This abnormal vascular reactivity caused an exaggerated BP response to mental and physical stress in an obese, normotensive, insulin-resistant population of women.
A potential explanation for this enhanced vasoconstriction in the IR group may be a lack of insulin-mediated vasodilation. Recent observations suggest that an impaired cellular response to insulin predisposes to increased vascular smooth muscle tone.21 In vitro and animal studies have shown that insulin has vasodilating properties, and insulin attenuates the vasoconstrictor and inotropic responses to various agonists.7 22 Thus, it appears that insulin normally modulates or attenuates vascular smooth muscle contractile responses to vasoactive substances and impaired insulin-mediated vasodilation may be instrumental in causing enhanced vasoconstriction in this study.
Insulin resistance accompanies compensatory hyperinsulinemia. Hence, hypertension in the insulin-resistant state generally has been attributed to hyperinsulinemia with resultant increases in sympathetic nervous system activity. However, we did not observe significant hemodynamic changes after acute glucose loading in either the IR or control group. Thus, this indicates that transient hyperinsulinemia does not affect hemodynamics. Our data are consistent with the findings of other investigators. Hall et al23 failed to observe an increase in BP when normal dogs were given a chronic infusion of insulin with or without norepinephrine. Anderson et al24 reported that modest increases in plasma insulin with euglycemia produced marked increases in muscle sympathetic nerve activity and plasma norepinephrine levels in normotensive individuals. Despite this sympathetic stimulation, forearm vascular resistance fell and mean arterial pressure did not rise. Similarly, Berne et al25 also demonstrated that insulin increased muscle sympathetic nerve activity and plasma norepinephrine levels without significant changes in arterial pressure.
A possible physiological role for insulin-mediated vasodilatation has been suggested by Laakso et al.26 They have demonstrated that insulin resistance in the skeletal muscle of obese individuals is partly due to a reduced response of skeletal muscle blood flow to insulin. Their findings prompted the speculation that insulin reduces vascular resistance and increases blood flow in skeletal muscle. Thus, resistance to the vasodilator effects of insulin rather than hyperinsulinemia may be primarily responsible for the abnormal vascular reactivity shown by our IR group. However, effects of chronic hyperinsulinemia on vascular smooth muscle should not be excluded. Hyperinsulinemia has been reported to increase renal sodium retention and enhance plasma renin activity, which may elevate intracellular free calcium in vascular smooth muscle, with consequent hypertrophy.27 28 Insulin and insulin-like growth factors are also mitogens capable of stimulating smooth muscle proliferation29 that could result in vascular smooth muscle hypertrophy and ultimately contribute to structural and functional changes. Established hypertension both with and without disturbances of glucose metabolism is characterized by increased systemic vascular resistance and normal or subnormal cardiac output. Our normotensive IR group exhibited enhanced vasoconstriction in response to stress, and this abnormal vascular reactivity may be an early indicator of the impairment of vascular smooth muscle that may lead to elevated vascular resistance.
Although the origin of insulin resistance is not clearly understood, insulin resistance is commonly found in otherwise healthy individuals. As many as 25% of the normal population are reported as being insulin resistant.30 One of the noteworthy findings of the present study is that a simple MAT or handgrip test raised BP to a hypertensive range in the majority of our healthy, normotensive IR group. This episodic increase in BP in response to psychological and physical stressors can have a significant effect on the cardiovascular system in this population. Previously, we reported that premenopausal women had a reduced BP response to mental stress and suggested vasodilator effects of estrogen in BP regulation in this population.31 In the present study, most of our IR subjects were premenopausal women; however, their BP response to stress was greatly exaggerated. This hyperreactivity may be a marker for future hypertension in an obese, normotensive, insulin-resistant population.
The current understanding of hypertension is that it is a syndrome of cardiovascular risk factors rather than a disease of numbers. This concept necessitates altering our approach to the management of hypertension. In addition to regular weight reduction and dietary consultation in the healthy, normotensive, insulin-resistant population, aggressive means of reducing insulin resistance may be indicated to prevent future hypertension and diabetes mellitus in this high-risk population.
Our IR group was significantly obese compared with the control group. Thus, obesity was an obvious confounder in this study. We had a difficult time finding normal-weight, IR subjects. Eighty percent of obese people were reported to be glucose intolerant, and the overlap of the two conditions cannot be avoided. Studies show that within obese populations, hyperinsulinemia correlates with BP.32 Furthermore, recent evidence indicates that insulin is associated with hypertension even in nonobese people,33 suggesting a more definite role of insulin resistance in BP regulation. In the present study, body weight was significantly associated with baseline diastolic BP, fasting glucose, and insulin levels but not with changes in BP during stress. However, our study group reflected more mild to moderate obesity, not severe obesity. In this range, plasma insulin levels and the glucose-to-insulin ratio were significant predictors of changes in BP during stress. Because of the relatively small sample size of the present study, the results need to be confirmed with a larger study population.
In summary, we have demonstrated that insulin resistance is associated with an exaggerated BP response to mental and physical stress in obese, normotensive women. The underlying mechanism mediating this response was enhanced vasoconstriction, which may be caused by reduced insulin-mediated vasodilation. In addition to resistance to the vasodilator effects of insulin, resultant chronic hyperinsulinemia may also contribute to structural and functional changes in smooth muscle. Our study also demonstrated that an abnormal vascular reactivity is already present in obese, normotensive, insulin-resistant women before established hypertension and thus may be a marker for future hypertension.
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Acknowledgments |
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We thank Wendy Orlowski, RN, and Mary Bateson, RN, for their assistance in this investigation.
Received September 18, 1996; first decision March 6, 1997; accepted March 17, 1997.
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