Effects of stress on heart rate complexity--a comparison between short-term and chronic stress.

This study examined chronic and short-term stress effects on heart rate variability (HRV), comparing time, frequency and phase domain (complexity) measures in 50 healthy adults. The hassles frequency subscale of the combined hassles and uplifts scale (CHUS) was used to measure chronic stress. Short-term stressor reactivity was assessed with a speech task. HRV measures were determined via surface electrocardiogram (ECG). Because respiration rate decreased during the speech task (p<.001), this study assessed the influence of respiration rate changes on the effects of interest. A series of repeated-measures analyses of covariance (ANCOVA) with Bonferroni adjustment revealed that short-term stress decreased HR D2 (calculated via the pointwise correlation dimension PD2) (p<.001), but increased HR mean (p<.001), standard deviation of R-R (SDRR) intervals (p<.001), low (LF) (p<.001) and high frequency band power (HF) (p=.009). Respiratory sinus arrhythmia (RSA) and LF/HF ratio did not change under short-term stress. Partial correlation adjusting for respiration rate showed that HR D2 was associated with chronic stress (r=-.35, p=.019). Differential effects of chronic and short-term stress were observed on several HRV measures. HR D2 decreased under both stress conditions reflecting lowered functionality of the cardiac pacemaker. The results confirm the importance of complexity metrics in modern stress research on HRV.

Decrease in the plasma von Willebrand factor concentration following glucose ingestion: the role of insulin sensitivity.

Elevated plasma von Willebrand factor (vWF) concentration is thought to be associated with increased prevalence of cardiovascular events in the insulin resistance syndrome. We examined the effects of oral glucose challenge and accompanying metabolic and hemodynamic changes on vWF levels with respect to insulin sensitivity. Forty normotensive and hypertensive subjects (mean age +/- SD, 40 +/- 5 years) underwent a standard oral glucose tolerance test (OGTT). Plasma vWF antigen, glucose, insulin, catecholamines, and hemodynamics were measured at rest, and at 30, 60, 90, and 120 minutes after glucose intake. Insulin sensitivity was determined by the insulin sensitivity index (ISI(0,120)). Resting plasma vWF concentration was associated with screening systolic blood pressure (BP) (r =.43, P =.005). There were time effects for all variables of interest. While vWF antigen (P =.044), epinephrine (P =.003), and diastolic BP (P =.001) decreased after glucose challenge, norepinephrine (P =.009), systolic BP (P =.022), and heart rate (P <.001) increased. Decline in vWF (area under the curve) was associated with decrease in epinephrine (r =.46, P =.004) and with screening systolic BP (r =.45, P =.004). However, neither resting plasma vWF levels nor vWF decrease following glucose ingestion were significantly associated with the ISI(0,120.) The plasma vWF concentration decreases following glucose ingestion. While mechanisms underlying this phenomenon may relate to sympathetic nervous system function, they seem not related to insulin sensitivity. Endothelial dysfunction such as caused by hypertension rather than metabolic dysregulation per se may underlie the elevated plasma vWF concentration found with insulin resistance.

The hypercoagulable state in sleep apnea is related to comorbid hypertension.

OBJECTIVE: Obstructive sleep apnea (OSA) is associated with increased prevalence of atherosclerotic disease. A hypercoagulable state thought to underly atherosclerosis has been described in both OSA and systemic hypertension. We wondered about the respective contribution of apnea and hypertension to a hypercoagulable state. DESIGN: Eighty-seven subjects with symptoms suggestive of OSA, mean age 47 years (range 32-64 years), underwent polysomnography and blood pressure (BP) screening. OSA was diagnosed when respiratory disturbance index (RDI) > or = 15. Subjects having systolic BP (SBP) > 140 mmHg and/or diastolic BP (DBP) > 90 mmHg were classified as having hypertension. Three hypercoagulability markers were measured: thrombin/antithrombin III complex (TAT), fibrin D-dimer (DD), and von Willebrand factor antigen (vWF:ag). RESULTS: Analysis of variance and multiple linear regression were performed on the following four subject groups: (1) normotensive non-apneics (n = 19), (2) normotensive apneics (n = 38), (3) hypertensive non-apneics (n = 11), and (4) hypertensive apneics (n = 19). OSA (groups 2 and 4) had no significant main effect on hemostasis. Hypertensives (groups 3 and 4) had higher plasma levels of TAT (median/inter-quartile range, 148/59-188 versus 77/53-108 pmol/l; P = 0.009) and of DD (376/265-721 versus 303/190-490 ng/ml; P = 0.040) than normotensives (groups 1 and 2). Across all subjects, SBP was the only significant predictor of TAT (P = 0.001) and of DD (P = 0.004), whereas DBP was the only significant predictor of vWF:ag (P = 0.029). These findings persisted even after controlling for gender, age, body mass index, RDI, mean SaO2, and hematocrit. CONCLUSION: Hypercoagulability in OSA is mediated by comorbid hypertension and might account for high cardiovascular morbidity in OSA in general.

Continuous positive airway pressure normalizes cardiac autonomic and hemodynamic responses to a laboratory stressor in apneic patients.

OBJECTIVES: We examined the effect of continuous positive airway pressure (CPAP) treatment for sleep apnea on cardiac contractility, heart rate variability, and hemodynamics at rest and in response to a laboratory stressor. SUBJECTS AND INSTRUMENTATION: Forty-one apneic patients were studied on three occasions: before treatment, after 1 full night of CPAP treatment, and after 1 week of CPAP treatment. The subjects were randomly assigned to receive effective treatment or placebo. Contractility and hemodynamics were determined with impedance cardiography, and parasympathetic activity was assessed by analysis of heart rate variability. Measures were determined at rest and in response to a stressor. DESIGN AND RESULTS: For the cardiac sympathetic (contractility) measures (preejection period, cardiac acceleration index [CAI], and low-frequency/high-frequency ratio) significant interactions were found in the combination treatment (CPAP vs placebo) by study day (day 1, day 3, day 11) by test period (baseline, preparation, talking) [p < 0.01]. For these measures, there were no differences between the treatment groups or responses to the stressor on day 1. Levels in placebo-treated subjects did not change or respond on the subsequent study days. In the CPAP-treated subjects, there was a decrease in these indexes at baseline, which became significantly lower by day 11 (ie, CAI levels were 24 Omega/s(2), 22 Omega/s(2), and 14 Omega/s(2) on day 1, day 3, and day 11, respectively). These measures also became responsive to the stressor by showing increased sympathetic activity (CAI levels on day 11 were 14 Omega/s(2) at baseline, 32 Omega/s(2) during speech preparation, and 36 Omega/s(2) while speaking). The parasympathetic indexes, such as high-frequency power or band of heart rate variability as determined by spectral analysis, showed a significant day-by-treatment interaction (p < 0.005), whereas the CPAP- treated group had significantly more parasympathetic activity after 1 week of treatment. For the hemodynamic measures (stroke volume [SV], cardiac output, and systemic vascular resistance [SVR]), there were significant treatment-by-study day-by-test-period interactions (p < 0.01). SV and cardiac output increased across days, and SVR decreased in the CPAP-treated patients. CONCLUSIONS: These results indicate that CPAP normalizes contractility, increases cardiac vagal tone, and changes hemodynamic regulation from being resistance dominated to being cardiac dominated. Thus, after 1 week of treatment with CPAP, many of the indicators of poor cardiac functioning in apnea patients are improved.

Obstructive sleep apnea and hypertension: are peripheral chemoreceptors involved?

The mechanism of pathogenesis of hypertension in patients with obstructive sleep apnea (OSA) is unknown. Many investigators point to the high sympathetic nervous system activity (SNS) observed in OSA patients. However, there is no clear explanation as to the mechanism for the development of SNS hyperactivity in these patients. A common feature of patients with OSA is repetitive bouts of transient hypoxemia during sleep. Repetitive transient hypoxemia in rats has resulted in hypertension. In OSA patients, resolution of nocturnal hypoxemia with CPAP has corrected nocturnal and diurnal hypertension. Also, exposure to hyperoxia reduces blood pressure and sympathetic activity in OSA patients, but not in normals. These data suggest a significant role of peripheral chemoreceptors in the regulation of vascular tone. We hypothesize that peripheral chemoreceptors significantly contribute to the pathogenesis of hypertension in patients with OSA and that this is associated with chemoreceptor hyperactivity. This implies that correcting the intermittent nocturnal hypoxemia alone may prevent the cardiovascular morbidity associated with obstructive sleep apnea.

Does caffeine confound relationships among adrenergic tone, blood pressure and sleep apnoea?

The purpose of this study was to determine whether caffeine consumption confounds the relationship among adrenergic tone, as measured by urinary norepinephrine (NE), blood pressure (BP) and obstructive sleep apnoea (OSA). Data were analysed using correlation and regression analysis, analysis of covariance and t-tests. Subjects included normotensives and hypertensives with and without OSA: 38 men, 23 women, aged 30-60 y; 100-150% of ideal body weight; without other major illness. Patients were studied using polysomnography, caffeine consumption was assessed, 24-h urinary NE levels were examined and ambulatory BP was recorded. Patients with OSA (N=27) reported significantly greater caffeine consumption than those without OSA (N=34) (295 vs. 103 mg, P=0.010), but caffeine was not significantly correlated with their ambulatory BP. In contrast, NE excretion correlated with caffeine consumption (r=0.24, P=0.041), apnoea severity (r=0.65, P < 0.001) and BP (r=0.34, P < 0.005). Significant OSA-NE and BP-NE relationships remained even after controlling for caffeine consumption. Patients with OSA consumed nearly three times the amount of caffeine as patients without OSA. While caffeine partially explains the increased adrenergic tone in patients with OSA and the relationship between BP and NE, it does not appear to contribute significantly to the relationship between OSA and elevated BP.

Plasma epinephrine levels in hypertension and across gender and ethnicity.

Epinephrine (E) infusions raise blood pressure and there is an excess incidence of hypertension among males and blacks. However, reports of E levels by ethnicity, gender, and blood pressure status are inconsistent. Insensitive assays, variability in plasma E levels within individuals, and the small size of most studies have contributed to these conflicting reports. We measured plasma E levels in a large diverse sample of subjects, using a highly sensitive assay. A total of 361 individuals participated in the study: 61% were men and 39% women, 74% were normotensive and 26% hypertensive, 59% were white and 41% were black. Except for difference in blood pressure and body mass index between the normotensives and hypertensives, subjects had similar baseline characteristics and took no antihypertensive medications for at least five days prior to sampling. All blood samples were collected after resting for a least 30 minutes following the insertion of an indwelling i.v. catheter. Catecholamine levels were determined using a radioenzymatic assay (assay sensitivities for E and norepinephrine were 6 pg/ml and 10 pg/ml, respectively). An ethnicity by gender interaction was found (F(1,315) = 5.126, p = .024). Subsequent analysis revealed that white women had significantly lower basal plasma E levels than white men (p <0.001) and black women (p = 0.036). There were no significant differences in E levels between black men and women or between white men and black men. Uncorrected E levels were lower in normotensive than hypertensive subjects (p = .009) but this difference was not significant when corrected for body mass index (BMI). Uncorrected norepinephrine levels were higher in women than men (p = .03) but the difference was no longer significant when corrected for BMI. Plasma E levels were significantly lower among white women than men or black women. In contrast to prior studies, E levels were lower in hypertensives, but this may reflect obesity among hypertensives.

Impedance cardiography-derived hemodynamic responses during baroreceptor testing with amyl nitrite and phenylephrine: a validity and reliability study.

Baroreflex (BR) testing with phenylephrine (PE) and amyl nitrite (AN) provided an opportunity to evaluate the ability of impedance cardiography (IC) to track the rapid hemodynamic (HD) changes elicited by these drugs. The AN response was measured after inhalation and the PE response was measured after a bolus injection in 19 subjects on two occasions. High reliability was observed for all of the HD measures. Blood pressure (BP), peripheral resistance (PR), and preejection period (PEP) decreased significantly after administration of AN, whereas heart rate (HR) and cardiac output (Q) increased. BP and total PR increased significantly after administration of PE; HR and Q decreased and PEP did not change significantly. Stroke volume did not change significantly with either drug. The BR slope was reliably elicited with AN and PE. The IC and Finapres BP consistently detected short-term changes in HD responses to AN and PE. The pharmacological interventions demonstrated that IC measures followed the course predicted by the actions of the drugs. Change in PEP and dZ/dt reflected increased contractility. The BR sensitivity was also reproducible.

Race and sex differences in cardiovascular recovery from acute stress.

To evaluate the effects of race and gender on recovery, i.e. the relative return to baseline after a stress challenge, cardiovascular and catecholamine measures were examined before, during and after two standardized laboratory stressors (a speaking and a mirror tracing task) in a group of 85 Black and White men and women (mean age 35.6 years, range 20 to 52). For the speech task, White men showed the least systolic (p < 0.025) and diastolic (p < 0.05) blood pressure recovery as compared to Black men and women. For the mirror star tracing task, total peripheral resistance (p < 0.03) recovery was least for Whites as compared to Blacks and heart rate (p < 0.04) recovery was least for White women as compared to Black women and men. There were no significant group effects in terms of catecholamine recovery from either task. The findings extend prior studies on race and gender by suggesting that these same characteristics affect recovery from stressors.

The effects of the menstrual cycle, race, and gender on adrenergic receptors and agonists.

OBJECTIVE: To examine possible effects of race, sex, and the menstrual cycle on adrenergic receptors (beta 2 and alpha 2) and agonists. METHODS: Sixty-three normotensive black men and women and white men and women were studied twice, approximately 6 weeks apart. Women were studied once during the follicular phase and once during the luteal phase of the menstrual cycle. beta 2-Adrenergic receptors and adenylate cyclase activity were examined on lymphocytes, and alpha 2-adrenergic receptors were examined on platelets. Norepinephrine and epinephrine were determined in plasma. RESULTS: Women showed greater lymphocyte beta 2-receptor sensitivity (isoproterenol-stimulated cyclic adenosine monophosphate; p = 0.009). Women also showed greater postreceptor adenylate cycle activity independent of the beta-receptor (forskolin stimulation; p = 0.006). When these differences were controlled for, the gender-related differences in beta 2-receptor sensitivity were no longer evident. Black women had a reduced beta 2-receptor sensitivity in the luteal phase compared with the follicular phase, whereas white women showed no significant change (p = 0.018). Black subjects had lower lymphocyte beta 2-receptor density (Bmax) values than white subjects (p = 0.047). There were no significant effects on alpha 2-adrenergic receptors. CONCLUSION: The findings suggest that although there is no generalized effect of the menstrual cycle on adrenergic receptors in white women, such an effect may occur in black women. The findings also suggest that previously reported gender-related differences in beta 2-receptor sensitivity may be due to gender-related differences in postreceptor activity and not the beta 2-receptor per se.

Amphetamine use: return of an old scourge in a consultation psychiatry setting.

OBJECTIVE: Recreational use of amphetamine and its analogues has increased considerably during the last decade. The aim of this study was to determine possible demographic characteristics of amphetamine users and nonusers who were seen in psychiatric consultations on inpatient medical and surgery wards. METHOD: The authors examined data from 2,983 patients admitted to the University of California, San Diego, Medical Center and seen by consultation-liaison psychiatrists from January 1989 to June 1995. Amphetamine use was identified by the results of toxicological screening or patients' self-reports. RESULTS: Throughout the interval covered by the analysis, 8.7% of the patients with consultations were current amphetamine users. The percentage of users decreased from 9.1% in 1989 to 4.5% in 1992 but increased after that to reach 15.6% in the first half of 1995. The users were generally younger than the nonusers; they were typically male, white, single, uninsured, and unemployed. In comparison with nonusers, the users were more likely to have a past psychiatric history (outpatient treatment or inpatient admission) and a family history of psychiatric disorder. The users were more often admitted because of suicide attempts, had a higher probability of being HIV-positive, and were overrepresented in the psychiatric consultations requested by the departments of infectious diseases, obstetrics/gynecology, and trauma surgery. CONCLUSIONS: The high prevalence of amphetamine-using patients referred for psychiatric consultation is striking. Although young white men were especially likely to be users, there were users in all age groups, in nearly all hospital wards, and with a variety of psychiatric symptoms.

Menstrual cycle effects on catecholamine and cardiovascular responses to acute stress in black but not white normotensive women.

This study examined cardiovascular and catecholamine responses to two standardized laboratory stressors in 33 healthy age- and weight-matched black and white normotensive women (mean age, 32 years) during two phases of the menstrual cycle. Subjects were studied in a randomized order at the same time of day on two separate occasions approximately six weeks apart, once during the follicular phase (days 7 to 10 after menses) and once during the luteal phase (days 7 to 10 after the leutenizing hormone surge) of the menstrual cycle. Black women has higher systolic (P=.01) and diastolic (P=.01) pressures compared with white women. Black women showed greater diastolic pressure (P <.01) and plasma epinephrine (P <.05) responses to stress during the follicular compared with the luteal phase of the menstrual cycle; white women showed no significant changes in these variables. The findings extend the literature on race differences in responsivity to stress and indicate that in contrast to white women, reproductive hormones do influence cardiovascular and catecholamine responsivity to stress in black women.

Psychologic characteristics associated with acute stressor-induced leukocyte subset redistribution.

This study examined relationships between psychologic characteristics and enumerative immune responses to an acute laboratory stressor. Lymphocyte subsets were measured in 104 subjects at rest and following a 6-minute laboratory naturalistic speaking stressor. Multiple linear regression was utilized to assess relationships between immune reactivity (change scores) and anger expression, hostility, anxiety, depression, and stress. The task resulted in significant increases over baseline in WBC (p < 0.001), T-suppressor/cytotoxic CD8 cells (p = 0.010) natural killer CD56 cells (p < 0.0001), and CD57 (p < 0.0001) cells, and significant decreases in T-cells (p = 0.012), T-helper cells (p = 0.003), B-cells (p < 0.001), and the T-helper/suppressor ratio (p < 0.001). In general, the regression suggested that moderate associations exist between certain psychologic attributes and acute subset redistribution. For example, the increase in natural killer cell subsets was significantly negatively associated with anger expression, hostility, and depression. Suppressor/cytotoxic (CD8) cell reactivity was associated with baseline as well as with the task-induced changes in anxiety. B-cell (CD19) responses were related to the subject's age, expression of anger, and depression scores. As with the cardiovascular reactivity literature, these findings suggest that a relationship exists between certain psychologic characteristics such as anger and anxiety and immune reactivity to acute stress.

Altered cardiac contractility in sleep apnea.

Adrenergic regulation in sleep apnea is a complex process because adrenergic physiology is difficult to summarize with one measure. Furthermore, the role of the adrenergic system in sleep apnea is often confounded with hypertension, making interpretation difficult in hypertensive apneics. Sixty-six people with and without apnea and/or hypertension (all were off antihypertensive medication) participated in this study. Cardiac beta-adrenergic drive, as assessed by systolic time intervals, was examined at rest and in response to a mild laboratory stressor. These measures of cardiac contractility included the pre-ejection period, electrical systole (QT) interval and the cardiac acceleration index. At rest, apneics showed elevated myocardial contractility on all measures (p = 0.001). In response to the laboratory stressor, non-apneics showed an increase in cardiac beta-adrenergic drive (p = 0.001), whereas the contractility in apneics did not change or decreased relative to baseline. These findings suggest disrupted cardiac adrenergic regulation in people with sleep apnea. Apnea appears to increase resting sympathetic activity and down regulate beta2-adrenergic receptors. The downregulation of cardiac beta-adrenergic receptor activity may explain the inability of people with sleep apnea to respond with appropriate cardiac contractility to a mild perturbation.

The effect of hypoxia on baroreflexes and pressor sensitivity in sleep apnea and hypertension.

Many persons with sleep apnea are hypertensive. Forty-two subjects of similar age and weight were divided into four groups of hypertensives and normotensives with and without sleep apnea. All subjects had heart rate, blood pressure (BP), baroreflex sensitivity and pressor sensitivity to phenylephrine measured while breathing room air or 15% oxygen. Hypoxia raised heart rate and lowered BP in all groups (p < 0.001), with the greatest hypotensive effect among hypertensives. Hypertensives had blunted baroreflex sensitivity, and breathing a hypoxic mixture lowered baroreflex sensitivity of all four groups (p = 0.008). The apneic subjects tended to lower their baroreflex sensitivity more in response to hypoxia and also had an enhanced pressor response to phenylephrine, whether breathing room air or 15% oxygen. Episodes of sleep apnea lead to hypoxia, an initial period of hypotension and a subsequent increase in sympathetic nervous activity. Our studies suggest that apneics could have an exaggerated pressor sensitivity to norepinephrine. They might also have difficulty returning BP to normal levels, because hypoxia impaired baroreflexes.

Lymphocyte subset redistribution in response to acute experimental stress: effects of gender, ethnicity, hypertension, and the sympathetic nervous system.

This study examined demographic and adrenergic characteristics associated with enumerative immune responses to acute laboratory stress. Lymphocyte subsets and plasma catecholamines were measured in 110 subjects at rest and following a naturalistic speaking stressor. Lymphocyte beta 2-adrenergic receptor sensitivity and density were measured at rest. The speaking task caused marked increase in natural killer cells, T-suppressor/cytotoxic cells, total WBC, norepinephrine, and epinephrine and decreases in T-helper cells, B cells and the T-helper/suppressor ratio. Multiple regression analyses demonstrated that, in general, cellular immune responses were best predicted by a combination of lower basal norepinephrine, higher beta 2-adrenergic receptor sensitivity, and a greater stress-induced increase in norepinephrine. The findings suggest that traditional epidemiologic characteristics such as gender, ethnicity, and mild hypertension have limited influence on lymphocytosis. Rather, interindividual differences in sympathetic nervous system characteristics play a more prominent underlying role in acute cellular immune system activation.

Beta 2-adrenergic receptor characteristics in sleep apnea patients.

This study examined the relationship between sleep apnea and beta 2-adrenergic receptor characteristics. Using standard polysomnography, individuals were classified as either apneic (n = 15) or mild to nonapneic (n = 15) according to their respiratory disturbance index (RDI). Subjects were similar in terms of sodium excretion and blood pressure. Apneic subjects showed a decrease in beta 2-adrenergic receptor sensitivity (p = 0.01) [as determined by isoproterenol-stimulated cyclic adenosine 5'-monophosphate (AMP) production in lymphocytes] and an increased binding affinity to the beta receptor antagonist [125I]iodopindolol (p < 0.001). beta receptor density was also diminished in apneics, but not significantly (p = 0.08). Forskolin-stimulated cyclic AMP was not significantly different between the groups, indicating a similarity in postreceptor Gs-adenylate cyclase activation. Across all subjects, RDI was negatively correlated with beta receptor sensitivity (r = -0.35, p = 0.05) and Kd (r = -0.54, p < 0.01) and positively correlated with systolic blood pressure (r = 0.37, p < 0.05). The findings indicate that sleep apnea is associated with a diminished beta 2-adrenergic receptor function but no change in postreceptor components and suggest a mechanism for the high comorbidity between sleep apnea and hypertension.

Racial differences in epinephrine and beta 2-adrenergic receptors.

This study examined the effects of ethnicity and hypertension on beta 2-adrenergic receptors and on plasma catecholamines in a group of 77 unmedicated mildly hypertensive and normotensive men. Black hypertensive subjects had the most sensitive and white hypertensive subjects the least sensitive beta-receptors (as assessed by isoproterenol-stimulated cyclic AMP in lymphocytes [P = .02]). In contrast, postreceptor adenylate cyclase activation (as assessed by forskolin stimulation) was similar among groups. As with beta-receptor sensitivity, black hypertensive subjects had the highest beta-receptor density and white hypertensive subjects the lowest (P = .03). Blacks demonstrated lower plasma epinephrine values compared with whites (P = .03). Across all subjects, plasma epinephrine was negatively correlated with beta-receptor density (r = -.26, P < .05) and sensitivity (r = -.25, P < .05). There were no group differences in binding affinity to the beta-antagonist iodopindolol. The findings support the notion of increased beta-adrenergic receptors in hypertension in blacks.

Relationship of insulin, race, and hypertension with hemodynamic reactivity to a behavioral challenge.

Insulin is a modulator of blood pressure and may play a role in the pathogenesis of hypertension. This study examined the relationship between fasting insulin level and cardiovascular reactivity in hypertensive and normotensive black and white patients. Eighty-one patients were studied after 3 days of hospitalization on an isocaloric diet providing 200 mmol Na+ and 100 mmol K+ per day. Fasting insulin levels were determined on the morning of the second hospital day; a median split was used to determine high- and low-insulin groups. On the next day of hospitalization we examined blood pressure and hemodynamic responses to a speaking challenge. Hemodynamic responses were determined with impedance cardiography. Reactivity was studied as the percentage change from resting baseline. There were significant race by blood pressure level interactions for systolic and diastolic blood pressure reactivity (P < or = .01). Black hypertensives showed more blood pressure reactivity than either the white hypertensives or the white normotensives; black normotensives had less blood pressure reactivity than the other groups. Insulin grouping interacted with blood pressure level and race on the reactivity of the underlying hemodynamic measures (total peripheral resistance, stroke volume, and heart rate; P < or = .02). Fasting insulin level had no relationship to blood pressure reactivity. On the other hand, insulin level interacted with blood pressure level and race on the underlying hemodynamics controlling blood pressure, namely total peripheral resistance and stroke volume.(ABSTRACT TRUNCATED AT 250 WORDS)