Trait anger, cynical hostility and inflammation in Latinas: variations by anger type?

Anger and hostility are psychological factors that appear to play a salient role in relation to cardiovascular disease (CVD) risk; however, their association with risk within the Latino population remains relatively unexplored. The current study examined associations between overall trait anger, anger subdimensions (i.e., anger temperament and anger reaction) and cynical hostility with sICAM-1, a marker of cellular adhesion and systemic inflammation related to CVD risk, in a sample of 294 middleaged Mexican-American women. Results showed no association between trait anger or anger temperament and sICAM-1. Anger reaction was marginally associated with sICAM-1 (ß=4.77, p=.06). Cynical hostility was significantly associated with sICAM-1 (ß=5.89, p=.04) even after controlling for demographic, biological and behavioral covariates. The current study provides evidence that specific aspects of anger and hostility relate to physiological pathways that potentially influence CVD risk. Findings are discussed in light of contextual cultural factors.

Do circulating leucocytes and lymphocyte subtypes increase in response to brief exercise in children with and without asthma?

BACKGROUND: Exercise can alter health in children in both beneficial (eg reduced long-term risk of atherosclerosis) and adverse (eg exercise-induced asthma) ways. The mechanisms linking exercise and health are not known, but may rest, partly, on the ability of exercise to increase circulating immune cells. Little is known about the effect of brief exercise, more reflective of naturally occurring patterns of physical activity in children, on immune cell responses. OBJECTIVES: To determine whether (1) a 6-min bout of exercise can increase circulating inflammatory cells in healthy children and (2) the effect of brief exercise is greater in children with a history of asthma. METHODS: Children with mild-moderate persistent asthma and age-matched controls (n = 14 in each group, mean age 13.6 years) performed a 6-min bout of cycle-ergometer exercise. Spirometry was performed at baseline and after exercise. Blood was drawn before and after exercise, leucocytes were quantified and key lymphocyte cell surface markers were assessed by flow cytometry. RESULTS: Exercise decreased spirometry only in children with asthma, but increased (p<0.001) most types of leucocytes (eg lymphocytes (controls, mean (SD) 1210 (208) cells/microl; children with asthma, 1119 (147) cells/microl) and eosinophils (controls, 104 (22) cells/microl; children with asthma, 88 (20) cells/microl)) to the same degree in both groups. Similarly, exercise increased T helper cells (controls, 248 (60) cells/microl; children with asthma, 232 (53) cells/microl) and most other lymphocyte subtypes tested. By contrast, although basophils (16 (5) cells/microl) and CD4+ CD45RO+ RA+ lymphocytes (19 (4) cells/microl) increased in controls, no increase in these cell types was found in children with asthma. CONCLUSIONS: Exercise increased many circulating inflammatory cells in both children with asthma and controls. Circulating inflammatory cells did increase in children with asthma, but not to a greater degree than in controls. In fact, basophils and T helper lymphocyte memory transition cells did not increase in children with asthma, whereas they did increase in controls. Even brief exercise in children and adolescents robustly mobilizes circulating immune cells.

Sympathetic alterations after sodium restriction and short-term captopril administration.

OBJECTIVES: The purpose of this study was to examine the effects of short-term captopril therapy during sodium restriction on several markers of the sympathetic nervous system, including plasma norepinephrine, neuropeptide Y, beta-adrenergic receptors and cortisol. BACKGROUND: Recent studies suggest that the therapeutic effects of converting enzyme inhibitors involve not only the renin-angiotensin and prostaglandin systems but also the sympathetic system. METHODS: Twelve hypertensive and 20 normotensive men were studied after 2 5-day hospital stays during which they consumed a 10-mEq sodium diet and received captopril (25 mg twice daily) or placebo in a double-blind crossover study. RESULTS: Captopril decreased neuropeptide Y (p < 0.05) and angiotensin II (p < 0.01) and increased isoproterenol-stimulated cyclic adenosine monophosphate (AMP) in lymphocytes (p < 0.03), plasma norepinephrine (p < 0.02), cortisol (p < 0.05) and renin (p < 0.001) in both hypertensive and normotensive subjects. Hypertensive subjects had an increased beta-adrenergic receptor density (p < 0.02) and a greater decrease in diastolic blood pressure compared with normotensive subjects (p < 0.02). CONCLUSIONS: The results of this study suggest that the short-term therapeutic effects of captopril may involve concerted changes in key components of the sympathetic nervous system. These findings, such as decreased neuropeptide Y combined with increased norepinephrine and beta-adrenergic receptors, are compatible with the observation of increased cardiac output and decreased peripheral resistance after short-term angiotensin-converting enzyme inhibition.

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.

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.

Decreased angiotensin II response but unaltered cardiovascular pressor response to infused norepinephrine after sodium restriction and converting enzyme inhibition.

Although studies indicate that converting enzyme inhibitors such as captopril influence beta-adrenergic physiology, the data on alpha-adrenergic physiology is inconsistent. This study therefore examined the effects of captopril (50 mg/day for 5 days) during sodium restriction on the pressor response and on angiotensin II and neuropeptide Y levels to infused norepinephrine (0.01 to 0.1 micrograms/kg/min) in 17 hypertensive and 27 normotensive subjects. Angiotensin II increased significantly in response to infused norepinephrine during placebo administration (p < 0.001) but not during captopril administration (p = 0.15). Neuropeptide Y levels decreased in response to captopril (p = 0.02). Despite these changes the pressor response to infused norepinephrine was unchanged with captopril. These data support the conclusion that the antihypertensive action of captopril is unrelated to alterations in norepinephrine-mediated alpha-adrenergic pressor regulation. The finding of a decrease in neuropeptide Y levels may have relevance to the therapeutic effects of captopril.

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.

Psychological states and lymphocyte beta-adrenergic receptor responsiveness.

There is a complex interplay between psychological states and biochemical factors. beta-Adrenergic receptor responsiveness is altered in some patients with depression and anxiety disorders, but the relation between various psychological states and receptor function in a normal population is unknown. We measured lymphocyte beta-adrenergic receptor density (Bmax), sensitivity (cAMP ratio), the Profile of Mood States (POMS), and Spielberger State-Trait Anxiety Inventory (STAI) in 39 hypertensives and 81 normotensives. We examined correlations between log normalized receptor variables and psychological states. Log Bmax showed negative correlations with age and with POMS tension-anxiety, depression-dejection, and anger-hostility. Log cAMP ratio did not show significant correlations with POMS and STAI ratings. In step-wise multiple regression analyses, 36% of the variance in Bmax was accounted for by POMS tension-anxiety, and age. Our study suggests that increased POMS tension-anxiety was highly associated with down-regulation of beta-adrenergic receptors, even in subjects who do not have psychiatric illness. Numerous psychological states could be associated with changes of beta-adrenergic receptor responsiveness in a normal population.

Peripheral blood mononuclear cell-endothelial adhesion in human hypertension following exercise.

OBJECTIVE: To determine the effects of hypertension and exercise on interleukin-6 (IL-6) levels and mononuclear cell adhesion to endothelial cells. DESIGN: Twelve hypertensive and 33 normotensive volunteers were studied prior to and following exhaustive exercise. End points were stimulated IL-6 levels and peripheral blood mononuclear cell (PBMC) CD11a (LFA-1) expression and in vitro PBMC adhesion to human umbilical venous endothelial cells (HUVEC). RESULTS: In response to exercise, all subjects showed a significant increase in lymphocyte CD11a a density and in IL-6 levels (P < 0.001). Compared to normotensives, hypertensives showed significantly greater mean density of CD11a on lymphocytes (P< 0.05) and on monocytes (P < 0.05). In response to exercise, hypertensive subjects showed a twofold greater increase in IL-6 as compared to normotensives (+ 240 pg/ml versus + 123 pg/ml, respectively; P< 0.05). PBMC adhesion to HUVEC was increased in hypertensives but decreased in normotensives following exercise (P< 0.03). CONCLUSION: The findings suggest that exercise leads to increased mononuclear cell adhesion to endothelial cells in patients with hypertension, possibly through cytokine-induced activation of mononuclear cell CD11a. These findings, coupled with prior data indicating increased endothelial activation in hypertension, may be relevant to the increased risk of atherosclerosis in human hypertension.

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.

Leukocyte adhesion molecule expression and T cell naïve/memory status following isoproterenol infusion.

This study examined adhesion molecules on peripheral leukocytes following a 30-min infusion of the beta-adrenergic agonist isoproterenol in 23 healthy subjects. In response to isoproterenol, the number of CD8 +CD62L- T cells and both CD62L+ and CD62L-natural killer (NK) (CD3 CD16+ 56+) cells increased markedly in circulation (p < 0.001). In addition, the surface density of CD62L was significantly lower on both CD8+ and CD4+ T cells (p < 0.001). Plasma levels of soluble CD62L remained unchanged, arguing against an isoproterenol-induced shedding of L-selectin. In contrast to CD62L, the surface density of the beta2 integrin LFA-1 (CD11a) was higher on circulating lymphocytes (p < 0.001) (but not monocytes or lymphocytes) post-infusion. Isoproterenol also led to a mobilization of memory/activated CD8+CD29high T cells (p < 0.01), but had no significant effect on the number of circulating CD8+ CD45RA+ CD62L+ naïve T cells. beta blockade with the non-specific antagonist propranolol eliminated these isoproterenol-induced effects.

The effects of hypoxia and sleep apnea on isoproterenol sensitivity.

STUDY OBJECTIVES: To determine the effects of both apnea and hypoxia on beta-adrenergic receptor sensitivity. DESIGN: Cross-sectional study. SETTING: A clinical research center. PATIENTS: Forty-five normotensive and hypertensive sleep apnea patients (respiratory disturbance index >20) and non-apneic controls. MEASUREMENTS AND RESULTS: The chronotropic 25 dose (CD25), an in vivo measure of beta-adrenergic receptor sensitivity derived from the heart rate response to a graded infusion of isoproterenol, was determined while subjects breathed either a normoxic (21% O2, 79% N2) or a hypoxic (15% O2, 85% N2) gas mixture. Under normoxic conditions, apnea patients showed a significantly higher CD25 (lower beta-adrenergic receptor sensitivity) as compared to controls (5.9 microg, SD=2.1 versus 4.6 microg, SD=1.2, respectively; p=0.018). In response to hypoxia, apnea patients showed no change in CD25, while controls showed a significant increase in CD25 (beta-adrenergic receptor desensitization) (p=0.002), to a value comparable to the apneics' (5.6 microg, SD=2.0). CONCLUSION: The in vivo finding of reduced beta-adrenergic receptor sensitivity in sleep apnea patients is consistent with previous in vitro assessments of the beta-adrenergic receptor. The finding that apnea patients do not respond to hypoxia with a further receptor desensitization suggests that sleep apnea patients may have reached a threshold effect of hypoxia on the beta-adrenergic receptor. These findings may be relevant to the greater incidence of hypertension seen in patients with sleep apnea syndrome.

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.

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.

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.

Effect of continuous positive airway pressure and placebo treatment on sympathetic nervous activity in patients with obstructive sleep apnea.

STUDY OBJECTIVES: We studied the effect of continuous positive airway pressure (CPAP) treatment on sympathetic nervous activity in 38 patients with obstructive sleep apnea. DESIGN: Randomized, placebo-controlled trial. SETTING: Patients underwent polysomnography on three occasions in a clinical research center, and had BP monitored over 24 h at home. All of the patients had sleep apnea with a respiratory disturbance index (RDI) > 15. INTERVENTIONS: The patients were randomized blindly to CPAP or placebo (CPAP at ineffective pressure) treatment. MEASUREMENTS AND RESULTS: Prior to therapy, the number of apneas and the severity of nocturnal hypoxia correlated significantly with daytime urinary norepinephrine (NE) levels, but not nighttime urinary NE levels. CPAP treatment lowered daytime BP from 99 +/- 2 mm Hg to 95 +/- 3 mm Hg (mean +/- SEM) and nighttime BP from 93 +/- 3 mm Hg to 88 +/- 3 mm Hg. Placebo CPAP treatment decreased both day and night mean BP only 2 mm Hg. CPAP, but not placebo, treatment lowered daytime plasma NE levels by 23%, daytime urine NE levels by 36%, daytime heart rate by 2.6 beats/min, and increased lymphocyte beta(2)-adrenergic receptor sensitivity (all p < 0.05). The effect of CPAP treatment on nighttime urine NE levels and heart rate did not differ from placebo treatment. There was a suggestion of an effect of placebo CPAP treatment on nighttime measures, but not on daytime measures. CONCLUSION: We conclude that daytime sympathetic nervous activation is greater with more severe sleep apnea. CPAP treatment diminished the daytime sympathetic activation; the potential nighttime effect of CPAP treatment was obscured by a small placebo effect.

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.

Race affects the decline in blood pressure with hospitalization.

Hospitalization routinely lowers blood pressure (BP). This study examined the effects of race and psychologic characteristics on this phenomenon. Data are reported from two separate cohorts of hypertensive and normotensive black and white men and women who were studied following a stay at a clinical research center where sodium intake was held constant. Blacks (N = 88), as compared to whites (N = 77), showed consistently smaller declines in systolic BP (P < .01) following hospitalization (-11.6 mm Hg SBP v -19.5 mm Hg SBP, respectively). A multiple regression model that treated BP as a function of physiologic and psychologic attributes indicated that preadmission BP level, body mass index, stress level, and anger expression were related to the drop in systolic (r2 = 65%) and diastolic (r2 = 45%) BP brought about by hospitalization (P < .0001). In blacks, high environmental stress ratings were unrelated to the change in BP with hospitalization. In contrast, whites with high environmental stress ratings lowered their BP noticeably with hospitalization. Given that the reduction in BP with hospitalization can be similar to that attained with pharmacologic therapy, these findings may have a bearing on studies examining BP in the hospital.

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)

Regional chest wall impedance during nonrespiratory maneuvers.

To assess changes in total and regional chest wall properties during nonrespiratory maneuvers, we measured electromyographic activity of various chest wall muscles, esophageal pressure, and rib cage and abdominal surface displacements in six subjects before and during various static tasks. Subjects were seated at functional residual capacity, and quasi-sinusoidal forcing at the mouth (0.4 Hz, 500 ml) was imposed during the maneuver in the absence of active breathing. Magnitude of total chest wall impedance (magnitude of Zw) increased with effort during all maneuvers; changes in phase were small. Maneuvers involving primarily muscles of the neck and rib cage--holding a 10-kg weight, 10 kg of isometric tension between the arms, and isometric neck flexion--roughly doubled the magnitude of rib cage impedance (magnitude of Zrc) and, to a lesser degree, increased magnitude of diaphragm-abdomen impedance (magnitude of Zd-a). Unilateral and bilateral leg lifts, in addition to increasing magnitude of Zd-a, increased magnitude of Zrc. Passive 90 degrees rotation of the torso caused approximately 25% increases in magnitude of Zrc and magnitude of Zd-a; if the rotation was actively maintained by the trunk muscles, both regional impedances increased over 100%. Increases in magnitude of regional impedance were correlated to increases in regional electromyographic activity; changes in phase were small. Passive restriction of rib cage displacement by strapping increased magnitude of Zrc and magnitude of Zw but not magnitude of Zd-a, whereas abdominal strapping increased magnitude of Zd-a but did not affect magnitude of Zrc or magnitude of Zw.(ABSTRACT TRUNCATED AT 250 WORDS)