Peripheral Resistance Responses Research Articles

Enhanced total peripheral vascular responsiveness in hypertension accords with the amplifier hypothesis.

Increases in vascular resistance (or the reciprocal, vascular conductance) in response to constrictor drugs are amplified (or attenuated) in the hindquarter vascular bed of hypertensive rats and rabbits. However, such changes have not been observed for the total peripheral circulation. To assess whether the vascular amplifier applies to the total peripheral circulation in conscious hypertensive rabbits. Rabbits were implanted with a flow probe for measuring cardiac output, a left atrial catheter for infusing dilator (adenosine) and constrictor (methoxamine) drugs, and ear artery and vein catheters for measuring mean arterial pressure (MAP) and for giving ganglion blockade. Data from full dose-total peripheral resistance (TPR) or total peripheral conductance (TPC) response curves to adenosine and methoxamine were combined into a logistic function extending from near full dilatation to near maximum constriction. Changes in MAP induced by methoxamine and adenosine were markedly greater in the 'wrap' rabbits (those with renal cellophane wrapping) compared with the sham animals. In the 'wrap' rabbits, the slopes and ranges of the adenosine-TPR response curve and the methoxamine-TPC response curve were 200% and 60%, respectively, of sham values. These data show that TPR changes are amplified, and TPC changes attenuated, to dilator and constrictor stimuli. The relationship between dose-average vascular radius (r; based on Poiseuille's law) over the full range of vascular tone showed that r was narrower in hypertension, but, in contrast to TPR, the degree of narrowing was almost the same between maximum dilatation and constriction. The total peripheral circulation in experimental hypertension is a TPR amplifier, or TPC attenuator, in the rabbit, consistent with well-established data in the major vascular beds.

Central adiposity and hemodynamic functioning at rest and during stress in adolescents.

To examine the impact of central adiposity upon hemodynamic functioning at rest and during stress in adolescents. Cross-sectional, correlational study. 46 White and 49 Black normotensive adolescents with family histories of essential hypertension. Systolic and diastolic blood pressure (SBP, DBP), cardiac output and total peripheral resistance responses were assessed at rest, during postural change, video game challenge and forehead cold stimulation. Specific lower and higher waist-to-hip ratio (WHR) tertiles were created for each gender and then integrated for analyses. This resulted in a lower WHR tertile of 11 Whites and 21 Blacks and an upper WHR tertile of 15 Whites and 17 Blacks. No differences in age, gender or ethnicity proportions were found between tertile groups (all P > 0.21). The upper WHR group showed greater body weight, waist and hip circumferences, body mass index (BMI), triceps skinfold and body surface area (all P < 0.001). Controlling for peripheral (that is, triceps skinfold) and overall (that is, BMI) adiposity, the upper WHR group exhibited greater SBP (that is, peak response minus mean pre-stressor level) to all three stressors and greater DBP reactivity to postural change and cold pressor (all P < 0.05). Central adiposity appears to adversely influence hemodynamic functioning during adolescence. Underlying mechanisms responsible for these associations require exploration.

Stroke volume response to cycle ergometry in trained and untrained older men.

The aims of this study were threefold: (1) to investigate the stroke volume (SV) response of trained older male cyclists [Cyclists: 65 (2.1) years, n = 10] during incremental cycle ergometry (20 W.min-1); (2) to determine the SV dynamics and total peripheral resistance response of untrained, but healthy and active older male controls [ 66 (1.1) years; n = 10]; (3) to compare the maximum oxygen consumption (VO2max) and SV response of trained older male runners [Runners: 65 (3.4) years; n = 11] with that of age-matched Cyclists. Impedance cardiography was used to assess the response of cardiac output (CO), SV and total peripheral resistance to exercise involving cycle ergometry. The mean VO2max of the trained Cyclists [54 (1.6) ml.kg-1.min-1] was significantly higher (P < 0.05) than that of the Runner [48 (3.9) ml.kg-1.min-1], whereas both groups possessed a significantly higher VO2max than the CONTROLS [28 (1.3) ml.kg-1.min-1]. During exercise, at a heart rate of 90 beats.min-1, the SV of the Cyclists increased by 41%, that of the Runners increased by 47%, and that of the CONTROLS increased by 31%. However, the Cyclists' and Runners' SV response was significantly greater than that of the CONTROLS. The SV for cyclists and controls peaked at 30% of VO2max. This early increase in SV was a major factor underlying the increase in CO during exercise in both the trained and the untrained subjects. In addition, all three groups showed a significant decrease in total peripheral resistance throughout exercise. The finding that older male runners possessed a large exercise SV and high VO2max suggests that run training results in enhanced cardiovascular performance during cycle ergometry.

Effect of Fluid Ingestion on Orthostatic Responses Following Acute Exercise

Orthostatic tolerance is impaired following an acute bout of exercise. This study examined the effect of fluid ingestion following treadmill exercise in restoring the cardiovascular responses to an orthostatic stress. Five men (age, 29.6 +/- 3.4 yrs) were exposed to a graded lower body negative (LBNP) pressure protocol (0 to -50 mmHg) during euhydration without exercise (C), 20 minutes after exercise dehydration (D), 20 minutes after exercise and fluid ingestion (FI20), and 60 minutes after exercise and fluid ingestion (FI60). Fluid ingestion (mean +/- SE) consisted of water-ingestion equivalent to 50% of the body weight lost during exercise (520 +/- 15 ml). Exercise dehydration resulted in significantly higher heart rates (119 +/- 8 vs 82 +/- 7 bpm), lower systolic blood pressures (95 +/- 1.7 vs 108 +/- 2.3 mmHg), a smaller increase in leg circumference (3.7 +/- 4 vs 6.9 +/- 1.0 mm), and an attenuated increase in total peripheral resistance (2.58 +/- 1.2 vs 4.28 +/- 0.9 mmHg/L/min) at -50 mmHg LBNP compared to the C condition. Fluid ingestion (both 20 and 60), partially restored the heart rate, systolic blood pressure, and total peripheral resistance responses to LBNP, but did not influence the change in leg circumference during LBNP (4 +/- 0.3 for R20 and 2.8 +/- 0.4 mm for R60). These data illustrate the effectiveness of fluid ingestion on improving orthostatic responses following exercise, and suggest that dehydration is a contributing factor to orthostatic intolerance following exercise.

Parental history of hypertension and cardiovascular response to stress in black and white men

White offspring of hypertensives typically exhibit an elevated cardiovascular response to stress. Studies of Black offspring of hypertensives have been fewer, with inconsistent results. This may be due, in part. to incomplete characterizations of hemodynamic responses. This study examines cardiovascular reactivity in Black and White offspring of hypertensives with a particular focus on vascular resistance responses. A total of 62 healthy normotensive men, 41 with a parental history of hypertension (PH+: 21 Blacks, 20 Whites), and 21 without parental hypertension (PH-: 7 Blacks, 14 Whites) engaged in a series of laboratory tasks. Both Black and White PH+ participants exhibited elevated diastolic blood pressure (DBP) responses, but to different patterns of stressor tasks. Familial differences in total peripheral resistance response were also obtained for Black and White participants in a comparison across all tasks, but were particularly evident in tasks when PH+ participants had elevated DBP responses. These results suggest that a parental history of hypertension is an important moderator of cardiovascular, and in particular peripheral vascular, responses to stress in Black and White individuals.

Haemodynamic response to head-up tilt in elderly hypertensives and diabetics.

To examine the haemodynamic mechanism associated with postural hypotension (PH) in elderly people, haemodynamic response to head-up tilt was studied in 14 elderly hypertensives and 13 elderly diabetics. Hypertensives and diabetics were divided into those with or without PH, defined as > or = 10 mmHg decline in mean blood pressure in response to head-up tilt. There was no significant change in cardiac output in hypertensives or diabetics with PH, whereas there was a significant increase during tilt in hypertensives without PH (p < 0.0001) and diabetics without PH (p = 0.0054). Hypertensives without PH showed a significant decrease in total peripheral resistance in response to head-up tilt (p = 0.0043). In hypertensives with PH and in both diabetic groups, there was no change in total peripheral resistance in response to head-up tilt. There was no difference in ejection fractions or heart rate responses between subjects with and without PH in either disease group. The difference in cardiac output change was not explained by myocardial changes observed at echocardiography nor by heart rate response nor by differences in total peripheral resistance. The results suggest that an increase in cardiac output in response to changing posture may be more important than vasoconstriction in protecting elderly subjects from PH.

Effect of 6 months of exercise training on cardiovascular responses to head‐up tilt in the elderly

The purpose of this investigation was to evaluate the effect of 6 months of exercise training on cardiovascular responses to 70 degrees head-up tilt (HUT) in the elderly. Forty-four elderly men and women (ages 60-82 years) were assigned to endurance training alone (n = 18), endurance training in combination with selected resistance exercises (n = 17), or to a non-exercising control group (n = 9). Head-up tilt testing at the start (T1) and end (T2) of 26 weeks of training consisted of 30 min of supine rest, 15 min of 70 degrees HUT, and 15 min of supine recovery. Endurance training consisted of uphill treadmill walking or stair climbing exercise 3 times per week, 30-45 min/day, at 75-85% of maximal heart rate reserve. In addition, the endurance/resistance group completed one set of 8-15 repetitions of biceps curl (BC), triceps extension (TE), and leg press, 3 times per week. After 26 weeks, increases in VO2max averaged 16.2% and 12.3% for endurance and endurance/resistance groups, respectively. In addition, the endurance/resistance group increased BC and TE strength by 25.3% and 26.1%, respectively. Results from the HUT test indicated that only the endurance group increased supine resting stroke volume (SV) and cardiac output (Q) from T1 to T2; however, SV and Q during HUT were not augmented as a result of training. Training did not affect heart rate, blood pressure, or peripheral resistance responses at rest or during HUT in any of the groups. These results suggest that 6 months of endurance training, alone or in combination with selected resistance exercises, is not detrimental to blood pressure controlling mechanisms to head-up tilt in the elderly.

Consistency of children's hemodynamic responses to laboratory stressors

Hemodynamic responses to three standard laboratory stressors (i.e., postural change, video game, forehead cold) were evaluated in 341 children (170 males) who had a mean age of 11.2 ± 2.6 years. Inter-task consistency was evaluated for five physiological parameters for all stressor pairings. Evidence of consistency in systolic and diastolic blood pressure, heart rate, cardiac output, and total peripheral resistance responses to all three stressors was observed. The highest and most consistent correlations across stressors were observed for cardiac output and total peripheral resistance responses. The need for clarification in the categorization of laboratory stressors used to measure reactivity is discussed.

Carotid baroreflex control during hemorrhage in conscious and anesthetized dogs.

The hypothesis was tested that carotid baroreflex gain is increased after 20% hemorrhage. The baroreceptor reflex responses to changes in carotid sinus pressure (CSP) were measured in control, 20% hemorrhage, and reinfusion conditions in three experimental groups: conscious intact (n = 7), anesthetized intact (n = 8), and anesthetized vagotomized (n = 8) dogs. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), and calculated total peripheral resistance (TPR) responses to changes in CSP were measured. At any given CSP, MAP, CO, and SV all decreased significantly with the 20% hemorrhage, as reflected by a downward shift in the reflex characteristic curve with no change in overall reflex range or gain. In contrast, TPR and HR responses to CSP were not significantly altered by 20% hemorrhage; reflex curves and gains were comparable to control conditions. In the conscious intact dogs, the maximal reflex gain, Gmax, for the MAP response was -1.365 +/- 0.25, -1.298 +/- 0.33, and -1.324 +/- 0.25 in control, 20% hemorrhage, and reinfusion conditions, respectively, and was not significantly altered by hemorrhage. In the same group, the Gmax for the HR response was -1.792 +/- 0.65, -1.709 +/- 0.33, and -1.986 +/- 0.67 in control, 20% hemorrhage, and reinfusion conditions, respectively; baroreflex gain on HR was not increased with hemorrhage. Plasma arginine vasopressin (AVP), an increase in which has been proposed to augment baroreflex gain, increased from a control level of 0.98 +/- 0.27 to 9.66 +/- 2.67 pg/ml during 20% hemorrhage in the conscious intact dogs; despite the increase in plasma AVP during hemorrhage, augmentation of baroreflex gain was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Carotid, Not Aortic, Chemoreceptors Mediate the Fetal Cardiovascular Response to Acute Hypoxemia in Lambs

The fetal cardiovascular response to acute hypoxemia consists of a decrease in heart rate, a variable change in mean arterial pressure, and an increase in peripheral vascular resistance. This response is mediated by the arterial chemoreceptors. To determine whether chemoreceptors in the carotid artery or in the aorta mediate the fetal cardiovascular response to acute hypoxemia, we studied the response to acute hypoxemia in fetal lambs at 125 to 130 d of gestation after selective carotid (six fetuses) or aortic (five fetuses) denervation. One to 3 d after insertion of catheters, hypoxemia was induced by inflating a balloon occluder around the ewe's hypogastric artery or by giving the ewe 95% N2 and 5% O2 to breathe. The chemoreflex response was measured as decrease in heart rate per decrease in Hb O2 saturation. To validate our results, we also studied the response to chemical stimulation of the chemoreceptors by injection of sodium cyanide into the inferior vena cava. We found that carotid denervation abolished the heart rate and peripheral vascular resistance responses to hypoxemia but that aortic denervation did not. Responses after injection of sodium cyanide were similar to those seen during acute hypoxemia. We conclude that the carotid chemoreceptors, and not the aortic chemoreceptors, mediate the fetal cardiovascular response to acute hypoxemia.

Hemodynamic effects of high dietary intakes of sodium or chloride in the Dahl salt-sensitive rat.

In the Dahl salt-sensitive (Dahl-S) rat, a high sodium without chloride diet (NaAA) and a chloride without sodium diet ("X"Cl) do not increase arterial pressure to the same extent as a high NaCl diet. To explain these differences, hemodynamic responses to acute volume expansion were compared in conscious Dahl-S and Dahl salt-resistant (Dahl-R) rats fed either 7% NaCl, NaAA, or "X"Cl diets for 5 weeks. Before acute volume expansion, on each of the three diets, mean arterial pressures and total peripheral resistances were higher (p less than 0.01) in Dahl-S than in Dahl-R rats, and in Dahl-S, arterial pressure was higher (p less than 0.05 or less) on the 7% NaCl intake than on the other two diets. No group differences were found in cardiac index (thermodilution). Right atrial pressure was also elevated (p less than 0.01) in Dahl-S rats on the 7% NaCl diet. In response to acute volume expansion, arterial pressure did not change, and the decrement of total peripheral resistance was greater in Dahl-S rats than in Dahl-R rats on each of the three diets (p less than 0.05 or less). Assuming that reductions of peripheral resistance in response to acute volume expansion reflect withdrawal of sympathetic tone, these results suggest that sympathetic tone is increased comparably on each of the diets in Dahl-S rats. As suggested by the increased right atrial pressure, higher arterial pressure induced by 7% NaCl may be related to an expanded intravascular volume in conjunction with increased neural activity.

Baroreflex control of arterial blood pressure during involuntary diving in ducks (Anas platyrhynchos var.).

The dynamic role of arterial baroreceptors in control of mean arterial blood pressure (MAP), heart rate (HR), cardiac output (CO), hindlimb vascular (HLVR) and total peripheral (TPR) resistance responses to forced dives was investigated in acutely and chronically barodenervated ducks. To activate the baroreflex, the proximal end of one aortic nerve was stimulated electrically with bipolar electrodes that had been implanted under pentobarbital sodium anesthesia. Predive nerve stimulation caused CO to fall (by reducing HR; stroke volume remained constant), producing a decrease in MAP to half the prestimulation level. During diving (for 2.5-min periods) nerve stimulation did not affect HR and MAP after the first minute of submersion. Neither HLVR nor TPR contributed to the fall in MAP during aortic nerve stimulation before or during diving. The effects of nerve stimulation on HR and MAP were maintained to the end of dives in animals given 100% O2 to breathe before diving. In separate experiments, increasing arterial chemoreceptor input by perfusing one vascularly isolated carotid body with venous blood caused a reduction in the effects of aortic nerve stimulation on MAP. Arterial baroreceptors may thus act on HR to alter MAP early in the dive, but as the dive progresses the baroreflex is attenuated by an increase in peripheral chemoreceptor drive.

Reduced vascular excitatory responses to cardiopulmonary unloading in hypertensive patients with left ventricular diastolic dysfunction.

Physiological consequences of altered peak left ventricular diastolic filling rate in hypertension have not yet been fully assessed. The hypothesis that altered left ventricular diastolic filling rate interferes with inhibitory cardiopulmonary reflexes was tested. Normalized peak left ventricular diastolic filling rate was calculated from radionuclide ventriculography. Haemodynamic changes during lower body negative pressure (-5 to -40 mmHg) in nine hypertensive patients with slow normalized left ventricular filling rate (Group A) were compared with 16 hypertensive patients with normal normalized peak left ventricular diastolic filling rate and ten normal volunteers of the same age group. Baseline total peripheral resistance was higher in essential hypertension compared to normals but did not differ significantly between the two hypertensive groups. For data analysis, the levels of lower body negative pressure were grouped as low levels of -5 to -10, and -15 to -20 mmHg, an intermediate level of -25 mmHg, and high levels of -30 to -40 mmHg; the change in total peripheral resistance (from baseline) was less prominent in Group A compared to Group B and to normals (-1.4 +/- 1.7 [SE], -0.06 +/- 1.4, 1.1 +/- 1.2 and 4.5 +/- 2 u.M2 in Group A at the four consecutive levels of lower body negative pressure vs. 0.9 +/- 0.7, 3.8 +/- 0.9, 7.2 +/- 1.6, and 8.2 +/- 1.4 in Group B, and 2.0 +/- 0.7, 3.3 +/- 0.8, 4.9 +/- 0.8, and 5.6 +/- 1.0 in normals). The reductions in central venous pressure and in pulmonary wedge pressure were not significantly different among the three groups at the different levels of lower body negative pressure, but the reduction in cardiac output was smaller in patients with reduced dv/dt ratio than in the other two groups. The responses to the cold pressor test were similar in all subjects. We conclude that patients with essential hypertension and diastolic dysfunction have impaired total peripheral resistance responses to lower body negative pressure. This abnormality may reflect an alteration in cardiac baroreflexes secondary to left ventricular diastolic dysfunction, an influence of baseline sympathetic activity on the observed vascular responsiveness to lower body negative pressure, or primary differences among groups in the changes in cardiac output induced by similar levels of lower body negative pressure.

Ethnicity and Ambulatory Blood Pressure Measurement: Relationship to Clinic and Laboratory Measurements

African Americans have a higher prevalence of hypertension than white Americans. Morbid consequences of hypertensive disease are greater in blacks than whites. For members of high-risk groups such as blacks, ambulatory blood pressure monitoring may be useful in supplementing casual clinic measurements to prevent misdiagnosis, better characterize the temporal topography of blood pressure responses, and improve prediction of left ventricular hypertrophy, hypertensive complications, morbidity, and mortality. In conjunction with other data, laboratory experiments showing that African Americans as a group show greater peripheral resistance and slowed natriuretic responses to behavioral stressors than whites, appear to provide insights as to why blacks generally respond better to diuretics and calcium channel blockers than to beta-adrenergic antagonists or angiotensin-converting enzyme inhibitors. It is suggested that ambulatory blood pressure monitoring and behavioral tasks in the laboratory may help predict individual responsiveness to antihypertensive agents.

Myocardial and Peripheral Vascular Responses to Behavioral Challenges and Their Stability in Black and White Americans

The purpose of this study was to assess the short term stability of myocardial and peripheral vascular responses to behavioral challenges, and to compare the response patterns of Black and White men. Blood pressure and heart rate, as well as stroke volume, cardiac output, total peripheral resistance, and systolic time interval measures derived from the impedance cardiogram were obtained in 12 Black and 12 White men. These measures were taken prior to and during an evaluative speech stressor, a mirror star tracing task, and a forehead cold pressor test presented during two laboratory sessions scheduled two weeks apart. In general, total peripheral resistance and impedance-derived baseline measures showed acceptable reproducibility (G greater than .85). With a few exceptions, adequate reliability was also demonstrated for change (delta) scores. All tasks raised blood pressure responses above resting levels. Blacks demonstrated significantly greater increases in total peripheral resistance responses across tasks. Whites but not Blacks also revealed increases above baseline in cardiac output and contractility as estimated by the Heather Index. These findings are consistent with the view that Blacks show greater vascular responsiveness than Whites across a variety of tasks, but reveal less myocardial responsiveness.

Effect of blocking angiotensin II receptor subtype on rat sympathetic nerve function.

This study examined effects of nonpeptide angiotensin II (Ang II) receptor subtype antagonists on the interaction of sympathetic function and Ang II in pithed rats. Effects of spinal cord stimulation (0.5-4 Hz) and norepinephrine (0.3-3 micrograms/kg i.v.) on mean arterial pressure (recorded with a carotid arterial catheter), cardiac output (measured with an electromagnetic flowmeter and flow probe around the thoracic ascending aorta), total peripheral resistance, and heart rate were determined. The subtype 1-selective Ang II receptor antagonist losartan (previously known as DuP 753) at 10 mg/kg i.v. blocked the hemodynamic responses to Ang II at 1 microgram/kg i.v. It inhibited mean arterial pressure and total peripheral resistance responses but not cardiac output and heart rate responses to spinal cord stimulation. In contrast, it reduced mean arterial pressure and cardiac output responses but not total peripheral resistance and heart rate responses to intravenous norepinephrine. Given at 100 mg/kg i.v., the subtype 2-selective receptor antagonist PD123177 did not reduce hemodynamic responses to intravenous Ang II, spinal cord stimulation, and intravenous norepinephrine. These results suggest that endogenous Ang II facilitates the release of norepinephrine from sympathetic nerve terminals in the vasculature of pithed rats. Similar to the Ang II receptor in vascular smooth muscle, the prejunctional Ang II receptor in pithed rats appears to be of subtype 1.

Generalization of cardiovascular response: supportive evidence for the reactivity hypothesis

Cardiovascular responses were monitored while 36 subjects completed a battery of laboratory stressors comprising mental arithmetic, a reaction time task, a speech task, and the forehead cold pressor. Inter-task consistency was assessed for each of 6 physiological parameters for all task pairings. Considerable inter-task consistency for reactivity scores was seen among the psychological stressors for all variables. The question of such consistency between the cold pressor and the psychological tasks was then addressed. The pattern of consistency was not as clear-cut in this case. For systolic blood pressure and pre-ejection period, reactivity scores to the cold pressor did not correlate with those to any of the psychological tasks. In contrast, cardiac output and total peripheral resistance responses showed considerable consistency. The importance of determining the nature of the relationship between psychological and physical stressors is discussed.

An Evaluation of Three Blood Pressure Methods in a Stabilized Acute Trauma Population

Blood pressure values were evaluated in 30 acute adult trauma patients using two indirect methods, the bell and diaphragm components of the stethoscope, and one direct arterial method. K1, K4, and K5 measurements were taken 4 to 72 hours (M = 30) after admission when vital signs had stabilized. Data were collected using a random-zero (RZ) sphygmomanometer for indirect blood pressure and radial intraarterial cannula for direct blood pressure. The sequence of measurement was randomized and variables shown to alter blood pressure values were controlled. There was no overall significant difference in K1, K4, and K5 blood pressures among the three methods. These results suggest that when clinicians monitor variables such as the frequency response of arterial lines and peripheral vascular resistance, indirect blood pressure methods are reliable for use with stabilized trauma patients.

Cardiac and Blood Pressure Responses to Mental Stress in Reactive Hypertensives

To study the haemodynamic response to a standardized mental stress, we measured ascending aorta velocity using Doppler ultrasonography in 20 reactive ("white-coat") hypertensives and 20 age and sex matched normal controls (NC) familiar with the hospital setting. Reactive hypertensives (RH) had 3 office diastolic BP recordings between 90-110 mmHg and ambulatory BP less than 140/90 mmHg. The cardiac response to mental arithmetic was greater in RH than NC (minute distance, RH: +36.7 +/- 40.2% vs NC: +10.3 +/- 19%, p less than 0.05; peak velocity, RH: +8.4 +/- 16.5% vs NC: -1.4 +/- 11.9%, p less than 0.05), and there was a different peripheral resistance response (RH: -12.2 +/- 24.2% vs NC: +6.5 +/- 22%, p less than 0.05). We suggest that subjects with reactive hypertension have a strong cardiac response to mental stress and this could be a characteristic of this condition.

Temporal stability of the hemodynamics of cardiovascular reactivity

Cardiovascular responses to a competitive reaction-time task were monitored in 13 male subjects tested twice, 3 months apart. The temporal stability of blood pressure responses was in line with previous reports. However, in this study impedance cardiography permitted the investigation of the hemodynamic adjustments underlying the observed blood pressure responses. Analyses revealed that cardiac output and total peripheral resistance responses displayed temporal stability, indicating that subjects' blood pressure responses on the two occasions were the result of similar hemodynamic responses. These data thus extend the literature by demonstrating that the hemodynamic response pattern itself represents a stable individual differences variable.