Cardiovascular responses of Type A and Type B behavior patterns to visual stimulation during rest, stress and recovery

Differences in the cardiovascular responses of individuals with behavior patterns of Type A and Type B were investigated during rest, stress, and recovery by visual stimulation. Thirty healthy undergraduate and graduate students (mean age: 22.18+/-1.44 years) were categorized as Type A (N=14), or Type B (N=16) based on the Kwansei Gakuin's daily life questionnaire. The cardiovascular reactivity of all participants was repetitively monitored for 6 sessions, with each session comprising 3 conditional phases, viz., resting, stress, and post-stress recovery. A gray screen was displayed during resting, displeasure-evoking images were displayed under the stress condition, and video clips of a forest or a control image (a gray screen) were displayed during the recovery condition. When participants were subjected to different stimuli on a 42-inch plasma television screen in each session, electrocardiograms (ECG), impedance cardiograms and the blood pressure (BP) of the respective participants were continuously monitored. According to the results, Type A indicated higher sympathetic reactivity than Type B during resting and under stress. As such, Type A indicated a shorter pre-ejection period (PEP) level during resting and a greater cardiac output (CO) increase under stress than Type B. Furthermore, parasympathetic predominance and parasympathetic antagonism accompanying the enhanced sympathetic activity induced by the unpleasant stress images decreased heart rate (HR) in both Type A and Type B, although the decrease in Type A was relatively meager. Unlike previous studies, the present study demonstrated that Type A indicated more enhanced sympathetic reactivity than Type B in resting physiological arousal levels and visual stimulus-induced stress.     

Early gestation dexamethasone programs enhanced postnatal ovine coronary artery vascular reactivity

Excessive exposure of the fetus to maternally derived corticosteroids has been linked to the development of adult-onset diseases. To determine if early gestation corticosteroid exposure alters subsequent coronary artery reactivity, we administered dexamethasone (0.28 mg.kg(-1).day(-1)) to pregnant ewes at 27-28 days gestation (term being 145 days). Vascular responsiveness was assessed in endothelium-intact coronary and mesenteric arteries isolated from steroid-exposed and age-matched control fetal sheep at 123-126 days gestation and lambs at 4 mo of age. Lambs exposed to maternal dexamethasone had higher mean arterial blood pressures than the age-matched controls (93 +/- 3 vs. 83 +/- 5 mmHg, P < 0.05). Mesenteric arteries from the steroid-exposed fetuses displayed diminished responses to ANG II, relative to controls. In 4-mo-old lambs, prenatal dexamethasone exposure significantly increased coronary artery vasoconstriction to ANG II, ACh, and U-46619, but not KCl. In contrast, postnatal mesenteric artery reactivity was unaltered by steroid exposure. Compared with fetal mesenteric reactivity, postnatal mesenteric reactivity to ANG II, phenylephrine, and U-46619 was diminished, whereas the response to 120 mmol/l KCl was heightened. Coronary artery ANG II receptor protein expression was not significantly altered by steroid exposure in either age group. These findings demonstrate that early-gestation glucocorticoid exposure programs postnatal elevations in blood pressure and selectively enhances coronary artery responsiveness to second messenger-dependent vasoconstrictors. Glucocorticoid-induced alterations in coronary vascular smooth muscle structure or function may provide a mechanistic link between an adverse intrauterine environment and later cardiovascular disease.     

The inhibited power motive, type A behavior, and patterns of cardiovascular response during the structured interview and Thematic Apperception Test

The Type A behavior pattern and the inhibited power motive have been implicated in the development of coronary heart disease (CHD). Since it is widely believed that enhanced cardiovascular responsivity may be one mechanism by which individuals develop CHD, the present study examined the relationship of Type A behavior and the inhibited power motive to different patterns of cardiovascular response during two behavioral tasks. Forty-one (24 Type A's, 17 Type B's) male undergraduates underwent the Type A structured interview (SI) and the Thematic Apperception Test (TAT) while a broad range of cardiovascular functions were simultaneously recorded. Different patterns of cardiovascular response were observed during the SI and TAT, and Type A's showed a greater tendency than Type B's to exhibit increased heart rate (HR), systolic blood pressure (SBP), and forearm blood flow (FBF) during the SI and the preparatory phase (but not the story-telling phase) of the TAT. The inhibited power motive was not related to enhanced cardiovascular responsivity during the SI or TAT. The implications of these findings for the development of CHD are discussed.     

Individual differences in the physiological effects of forest therapy based on Type A and Type B behavior patterns

Background

In recent years, the physiological relaxation effects of natural environments have been widely exploited, and although individual differences in the effects of forest therapy are known, assessment methods have not been clearly established. This study used a classification based on Type A and Type B behavior patterns to explain individual differences in physiological responses to forest environments.

Methods

We performed physiological experiments in 44 forest and urban (controls) areas. In total, 485 male university students (age, 21.8 ± 1.6 years) participated in the study. The subjects were asked to visit forest or urban environments randomly and observe each landscape for 15 min. The subjects’ pulse rates and blood pressures were tested to evaluate their physiological responses. The Kwansei Gakuin daily life questionnaire was used to identify Type A and Type B behavior patterns in subjects.

Results

The pulse rate was significantly lower in the Type B group after exposure to forest areas than after exposure to urban areas, whereas no significant difference was observed in the Type A group. In addition, the pulse rate was significantly lower in the low scoring subjects in the Type B group, which was consistent with changes in their diastolic blood pressure.

Conclusions

These results suggest that individual differences in pulse rate and blood pressure in response to forest environments can be explained by Type A and Type B behavior patterns.     

Alpha-adrenoceptor-mediated coronary vasoconstriction is augmented during exercise in experimental diabetes mellitus.

This study tested whether alpha-adrenoceptor-mediated coronary vasoconstriction is augmented during exercise in diabetes mellitus. Experiments were conducted in dogs instrumented with catheters in the aorta and coronary sinus and with a flow transducer around the circumflex coronary artery. Diabetes was induced with alloxan monohydrate (n = 8, 40 mg/kg i.v.). Arterial plasma glucose concentration increased from 4.7 +/- 0.2 mM in nondiabetic, control dogs (n = 8) to 21.4 +/- 1.9 mM 1 wk after alloxan injection. Coronary blood flow, myocardial oxygen consumption (MVo(2)), aortic pressure, and heart rate were measured at rest and during graded treadmill exercise before and after infusion of the alpha-adrenoceptor antagonist phentolamine (1 mg/kg iv). In untreated diabetic dogs, exercise increased MVo(2) 2.7-fold, coronary blood flow 2.2-fold, and heart rate 2.3-fold. Coronary venous Po(2) fell as MVo(2) increased during exercise. After alpha-adrenoceptor blockade, exercise increased MVo(2) 3.1-fold, coronary blood flow 2.7-fold, and heart rate 2.1-fold. Relative to untreated diabetic dogs, alpha-adrenoceptor blockade significantly decreased the slope of the relationship between coronary venous Po(2) and MVo(2). The difference between the untreated and phentolamine-treated slopes was greater in the diabetic dogs than in the nondiabetic dogs. In addition, the decrease in coronary blood flow to intracoronary norepinephrine infusion was significantly augmented in anesthetized, open-chest, beta-adrenoceptor-blocked diabetic dogs compared with the nondiabetic dogs. These findings demonstrate that alpha-adrenoceptor-mediated coronary vasoconstriction is augmented in alloxan-induced diabetic dogs during physiological increases in MVo(2).     

Cardiodynamic response to psychological and cold pressor stress: Further evidence for stimulus response specificity and directional fractionation

In the present study 36 police officers were exposed to a psychological stressor (IQ quiz) and to cold pressor stress while several cardiovascular variables were monitored. Impedance cardiography was used to provide measures of heart rate, stroke volume, cardiac output, myocardial contractility, and total peripheral resistance. In addition, measures of systolic and diastolic blood pressure and peripheral skin temperature were obtained. A multivariate analysis of variance (MANOVA) indicated that significant increases in diastolic and systolic blood pressure during the cold pressor test were mediated by large increases in total peripheral resistance, whereas blood pressure elevation during the IQ quiz were accompanied by significant increases in heart rate and, to a lesser extent, cardiac output. Peripheral skin temperature decreased in response to each stressor. Additional analysis indicated a degree of stimulus specificity for several variables. For example, diastolic blood pressure showed greater increases to cold pressor than quiz, whereas systolic blood pressure increased more with the psychological than the physical stressor. Directional fractionation occurred for both myocardial contractility and cardiac output.     

Cardiodynamic response to psychological and cold pressor stress: further evidence for stimulus response specificity and directional fractionation

In the present study 36 police officers were exposed to a psychological stressor (IQ quiz) and to cold pressor stress while several cardiovascular variables were monitored. Impedance cardiography was used to provide measures of heart rate, stroke volume, cardiac output, myocardial contractility, and total peripheral resistance. In addition, measures of systolic and diastolic blood pressure and peripheral skin temperature were obtained. A multivariate analysis of variance (MANOVA) indicated that significant increases in diastolic and systolic blood pressure during the cold pressor test were mediated by large increases in total peripheral resistance, whereas blood pressure elevation during the IQ quiz were accompanied by significant increases in heart rate and, to a lesser extent, cardiac output. Peripheral skin temperature decreased in response to each stressor. Additional analysis indicated a degree of stimulus specificity for several variables. For example, diastolic blood pressure showed greater increases to cold pressor than quiz, whereas systolic blood pressure increased more with the psychological than the physical stressor. Directional fractionation occurred for both myocardial contractility and cardiac output.     

Changes in blood pressure, heart rate and blood constituents during heat exposure in men with elevated blood pressure

Although the vascular volume response of hypertensive men during exercise has been rather well characterized, the effect of resting heat exposure in this patient population has not been examined. This was done in the present report in seven men with high blood pressure (BP) (i.e., diastolic pressure greater than 12 kPa (90 mmHg) upon initial interview) and 5 normotensive control subjects. 50 min after each subject had consumed an amount of water equal to 1% of his body weight, he reclined on a cot. 10 min later the subject was carried into an environmental chamber equilibrated at Tdb = 45 degrees C, Twb = 28 degrees C. Free-flowing venous blood samples were obtained from a cubital vein, and BP and heart rate were measured, before the heat exposure and at 15 min intervals during the experiment. Within 30 min systolic, diastolic and mean BP of the high BP subjects had decreased to normal levels; no BP changes were detected in normotensive subjects. Accompanying this depressor response was an exaggerated elevation in plasma glucose concentration. No alterations were found with haematocrit, plasma osmolality or electrolytes, or total protein and albumin. The data suggest that heat exposure may have been more stressful for the subjects with high BP than for their controls. This finding implies that phasic depressor responses may be as important as phasic pressor episodes in the aetiology of established essential hypertension.     

Regional myocardial O2 consumption and coronary blood flow responses to acetylcholine in rabbit heart

The effect of acetylcholine on regional coronary blood flow and myocardial O2 consumption was determined in order to compare its direct vasodilatory effects with the metabolic vasoconstriction it induces. Experiments were conducted in seven untreated control anaesthetized open chest rabbits and seven rabbits which were infused with acetylcholine (1 microgram/kg/min). Myocardial blood flow was determined before and during acetylcholine infusion using radioactive microspheres. Regional arterial and venous O2 saturation was analyzed microspectrophotometrically. Acetylcholine reduced heart rate by 30% and significantly depressed the arterial systolic and diastolic blood pressure. The mean O2 consumption was significantly reduced with acetylcholine from 9.6 +/- 2.0 to 6.1 +/- 3.6 ml O2/min/100 g. Coronary blood flow decreased uniformly across the left ventricular wall by about 50% and resistance to flow increased by 42% despite potential direct cholinergic vasodilation. O2 extraction was not affected by acetylcholine infusion. It is concluded that the acetylcholine infusion directly decreased myocardial O2 consumption, which in turn lowered the coronary blood flow and increased the resistance. The decreased flow was related to a reduced metabolic demand rather than a direct result of lowered blood pressure. Unaffected myocardial O2 extraction also suggested that blood flow and metabolism were matched. This indicates that direct cholinergic vasodilation of the coronary vasculature does not allow a greater reduction in metabolism than flow in the anaesthetized open chest rabbit heart during acetylcholine infusion.     

Adenosine is not responsible for local metabolic control of coronary blood flow in dogs during exercise

The purpose of this investigation was to quantitatively evaluate the role of adenosine in coronary exercise hyperemia. Dogs (n = 10) were chronically instrumented with catheters in the aorta and coronary sinus, and a flow probe on the circumflex coronary artery. Cardiac interstitial adenosine concentration was estimated from arterial and coronary venous plasma concentrations using a previously tested mathematical model. Coronary blood flow, myocardial oxygen consumption, heart rate, and aortic pressure were measured at rest and during graded treadmill exercise with and without adenosine receptor blockade with either 8-phenyltheophylline (8-PT) or 8-p-sulfophenyltheophylline (8-PST). In control vehicle dogs, exercise increased myocardial oxygen consumption 4.2-fold, coronary blood flow 3.8-fold, and heart rate 2.5-fold, whereas mean aortic pressure was unchanged. Coronary venous plasma adenosine concentration was little changed with exercise, and the estimated interstitial adenosine concentration remained well below the threshold for coronary vasodilation. Adenosine receptor blockade did not significantly alter myocardial oxygen consumption or coronary blood flow at rest or during exercise. Coronary venous and estimated interstitial adenosine concentration did not increase to overcome the receptor blockade with either 8-PT or 8-PST as would be predicted if adenosine were part of a high-gain, negative-feedback, local metabolic control mechanism. These results demonstrate that adenosine is not responsible for local metabolic control of coronary blood flow in dogs during exercise.     

Health patterns associated with type A behavior: a managerial population.

Type A Behavior is a behavioral syndrome found to be related to coronary heart disease and characterized by excessive drive, ambition, and competitiveness. Managers from 12 different companies were examined for this syndrome and for a number of the known risk factors in coronary heart disease (blood pressure, cholesterol, triglycerides, uric acid, smoking, and fitness). Those individuals exhibiting extreme Type A Behavior (Type A) showed significantly higher blood pressure (systolic and diastolic) and higher cholesterol and triglyceride levels. A greater percentage of these individuals were cigarette smokers. On serum uric acid there were no differences. In each age group, Type A's were less interested in exercise, although differences in cardio-respiratory fitness were found only in the oldest age group. Type A Behavior also was related to age, education, company growth rates, and stress symptoms. Overall, the Type A1's were found to be higher on a number of risk factors known to be associated with coronary heart disease. With regard to the Type A2's (individuals with less developed Type A Behavior), the findings were not conclusive.     

Plasma ATP during exercise: possible role in regulation of coronary blood flow

It was previously shown that red blood cells release ATP when blood oxygen tension decreases. ATP acts on microvascular endothelial cells to produce a retrograde conducted vasodilation (presumably via gap junctions) to the upstream arteriole. These observations form the basis for an ATP hypothesis of local metabolic control of coronary blood flow due to vasodilation in microvascular units where myocardial oxygen extraction is high. Dogs (n = 10) were instrumented with catheters in the aorta and coronary sinus, and a flow transducer was placed around the circumflex coronary artery. Arterial and coronary venous plasma ATP concentrations were measured at rest and during three levels of treadmill exercise by using a luciferin-luciferase assay. During exercise, myocardial oxygen consumption increased approximately 3.2-fold, coronary blood flow increased approximately 2.7-fold, and coronary venous oxygen tension decreased from 19 to 12.9 mmHg. Coronary venous plasma ATP concentration increased significantly from 31.1 to 51.2 nM (P < 0.01) during exercise. Coronary blood flow increased linearly with coronary venous ATP concentration (P < 0.01). Coronary venous-arterial plasma ATP concentration difference increased significantly during exercise (P < 0.05). The data support the hypothesis that ATP is one of the factors controlling coronary blood flow during exercise.     

Circadian blood pressure rhythm in primary and secondary hypertension.

Circadian blood pressure variability was recorded in patients with primary hypertension and with different forms of secondary hypertension using ambulatory 24-h blood pressure measurement. A group of 20 patients with different forms of secondary hypertension was compared with a matched group of patients with primary hypertension. Although the mean 24-h blood pressure was not different between the two groups, the patients with secondary hypertension had significantly higher systolic blood pressure during sleep and higher systolic and diastolic blood pressure in the early morning, compared with the primary hypertension group. This nocturnal blood pressure fall was then investigated in various groups of patients with different forms of secondary hypertension and compared with normotensives and patients with primary hypertension. Patients with mild primary hypertension (n = 152) and with severe primary hypertension (n = 30) had the same blood pressure fall (14-16 mm Hg systolic and diastolic) during the night (23:00-05:00 h) as normotensives (n = 20). However, in patients with renoparenchymal hypertension (n = 29), renovascular hypertensions (n = 20), hyperaldosteronism (n = 6), and hyperthyroidism (n = 14), the nocturnal blood pressure fall was significantly (p less than 0.01) reduced. One patient with coarctation of the aorta and nine patients with primary hyperparathyroidism and elevated blood pressure had a normal circadian blood pressure profile with a normal nocturnal blood pressure fall. The heart rate decrease during the night was equal in all patient groups. Ambulatory blood pressure measurement allows blood pressure recording under everyday conditions, including nighttime. In primary hypertension the blood pressure variability exhibits the same circadian variation as in normotension, showing a marked nocturnal fall.(ABSTRACT TRUNCATED AT 250 WORDS)     

Matrix metalloproteinases and membrane damage markers in sera of patients with acute myocardial infarction

Coronary artery disease is a multifunctional disease and represents one of the leading causes of death worldwide. Oxidative stress appears as an etiological factor for myocardial damage during acute myocardial infarction. Some data suggest that acute coronary syndromes may also be influenced by matrix metalloproteinases through degradation of the fibrous cap of vulnerable atherosclerotic lesions. It has been indicated that gelatinases A and B play a key role in acute myocardial infarction and deoxyribonuclease I has been postulated to be a novel early phase marker of disease. The aim was to study activity of gelatinases A and B in acute myocardial infarction and its association with some membrane damage markers. Seventy-five patients with disease and seventy-five healthy controls were enrolled. Activities of lactate dehydrogenase, malate dehydrogenase, and deoxyribonuclease I were estimated using standard spectrophotometric assay and isoforms of lactate and malate dehydrogenases were determined using direct zymography. Activity of dehydrogenases was significantly higher in patients, while deoxyribonuclease I was lower. Isoform 2 of lactate dehydrogenase was significantly higher in the patient group. Gelatinases A and B were detected only in patients group. The results suggest determination of serum malate dehydrogenase activity to be used as an additional parameter for acute myocardial infarction diagnosis. Those findings suggest important role of gelatinases A and B as biomarkers of early stage of acute myocardial infarction together with membrane damage parameters.     

Differing physiological effects of epinephrine in type 1 diabetes and nondiabetic humans

Acute increases of the key counterregulatory hormone epinephrine can be modified by a number of physiological and pathological conditions in type 1 diabetic patients (T1DM). However, it is undecided whether the physiological effects of epinephrine are also reduced in T1DM. Therefore, the aim of this study was to determine whether target organ (liver, muscle, adipose tissue, pancreas, cardiovascular) responses to epinephrine differ between healthy subjects and T1DM patients. Thirty-four age- and weight-matched T1DM (n = 17) and healthy subjects (n = 17) underwent two randomized, single-blind, 2-h hyperinsulinemic euglycemic clamp studies with (Epi) and without epinephrine infusion. Muscle biopsy was performed at the end of each study. Epinephrine levels during Epi were similar in all groups (4,039 +/- 384 pmol/l). Glucose (5.3 +/- 0.06 mmol/l) and insulin levels (462 +/- 18 pmol/l) were also similar in all groups during the glucose clamps. Glucagon responses to Epi were absent in T1DM and significantly reduced compared with healthy subjects. Endogenous glucose production during the final 30 min was significantly greater during Epi in healthy subjects compared with T1DM (8.4 +/- 1.3 vs. 4.4 +/- 0.6 micromol.kg(-1).min(-1), P = 0.041). Glucose uptake showed almost a twofold greater decrease with Epi in healthy subjects vs. T1DM (Delta31 +/- 2 vs. Delta17 +/- 2 nmol.kg(-1).min(-1), respectively, P = 0.026). Glycerol, beta-hydroxybutyrate, and nonesterified fatty acid (NEFA) all increased significantly more in T1DM compared with healthy subjects. Increases in systolic blood pressure were greater in healthy subjects, but reductions of diastolic blood pressure were greater in T1DM patients with Epi. Reduction of glycogen synthase was significantly greater during epinephrine infusion in T1DM vs. healthy subjects. In summary, despite equivalent epinephrine, insulin, and glucose levels, changes in glucose flux, glucagon, and cardiovascular responses were greater in healthy subjects compared with T1DM. However, T1DM patients had greater lipolytic responses (glycerol and NEFA) during Epi. Thus we conclude that there is a spectrum of significant in vivo physiological differences of epinephrine action at the liver, muscle, adipose tissue, pancreas, and cardiovascular system between T1DM and healthy subjects.     

Urinary dopamine, noradrenaline and adrenaline in type 2 diabetic patients with and without nephropathy

We measured the urinary excretions of dopamine, noradrenaline and adrenaline, their conjugated metabolites, urinary excretion of sodium and creatinine clearance simultaneously in 21 patients with Type 2 (non-insulin-dependent) diabetes and 6 normal subjects. The mean (+/- SEM) value for urinary excretion of dopamine (52.4 +/- 8.8 micrograms/day) in diabetic patients with nephropathy (Group C, n = 12) was significantly lower (P less than 0.01) than in the normal subjects (Group A, 179.7 +/- 15.5 micrograms/day) and in diabetic patients without nephropathy (Group B, n = 9, 131.5 +/- 16.5 micrograms/day). The mean values for the urinary excretions of noradrenaline and adrenaline were also significantly lower (P less than 0.01) in Group C than in Groups A and B. In addition, the mean urinary excretion of conjugated metabolite of dopamine in Group C was significantly lower (P less than 0.05) than in Group A. There was a trend toward the observation that the mean 24-h urinary excretion of sodium in Group C (121.6 less than 12.9 mEq) was lower as compared with that in Group A (140.8 +/- 8.9 mEq) or B (150.7 +/- 17.9 mEq). A multiple regression analysis revealed that the 24-h urinary excretion of dopamine correlated significantly with creatinine clearance, systolic (P less than 0.01) and diastolic (P less than 0.05) blood pressures. The results indicate that synthesis or secretion of renal dopamine might decrease with a progression of diabetic nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alpha tocopherol supplementation decreases serum C-reactive protein and monocyte interleukin-6 levels in normal volunteers and type 2 diabetic patients

Type 2 diabetic subjects have an increased propensity to premature atherosclerosis. Alpha tocopherol (AT), a potent antioxidant, has several anti-atherogenic effects. There is scanty data on AT supplementation on inflammation in Type 2 diabetic subjects. The aim of the study was to test the effect of RRR-AT supplementation (1200 IU/d) on plasma C-reactive protein (CRP) and interleukin-6 (IL-6) release from activated monocyte in Type 2 diabetic patients with and without macrovascular complications compared to matched controls. The volunteers comprised Type 2 diabetic subjects with macrovascular disease (DM2-MV, n = 23), Type 2 diabetic subjects without macrovascular complications (DM2, n = 24), and matched controls (C, n = 25). Plasma high sensitive CRP (Hs-CRP) and Monocyte IL-6 were assayed at baseline, following 3 months of supplementation and following a 2 month washout phase. DM2-MV subjects have elevated HsCRP and monocyte IL-6 compared to controls. AT supplementation significantly lowered levels of C-reactive protein and monocyte interleukin-6 in all three groups. In conclusion, AT therapy decreases inflammation in diabetic patients and controls and could be an adjunctive therapy in the prevention of atherosclerosis.     

Distension of urinary bladder induces exaggerated coronary constriction in smokers with early atherosclerosis

Distension of the urinary bladder causes an increase in efferent sympathetic activity, which can precipitate myocardial ischemia. Smoking has been shown to modulate activities of afferent nerves from the distended urinary bladder and to impair endothelial function in response to sympathetic activation. To assess the effect of bladder distension on coronary dynamics in smokers, we measured epicardial and microvascular responses in 24 patients with early atherosclerosis (< 50% diameter stenosis). Patients were classified into habitual smokers (group 1, n = 14) and nonsmokers (group 2, n = 10). Habitual smokers were randomized into two subgroups on the basis of the use of doxazosin, as follows: subgroup 1A (n = 7), without administration of doxazosin before catheterization; subgroup 1B (n = 7), with dosing doxazosin. In response to bladder distension (mean intravesical pressure 21.5 mmHg), bladder distension significantly decreased coronary diameter at the stenotic segments, coronary blood flow, and increased coronary resistance compared with baseline values, in subgroup 1A patients. In subgroup 1B patients during bladder distension, coronary diameter, coronary blood flow, and coronary resistance did not show significant changes compared with baseline values. There were significant differences of coronary diameter at the stenotic segments, coronary blood flow, and of changes of coronary vascular resistance between subgroup 1A and group 2 during bladder distension, despite similar changes in rate-pressure product. The present study showed that urinary bladder distension caused an abnormal vasomotor response of epicardial vasoconstriction and a concomitant increased coronary resistance, which leads to reduction in coronary blood flow in patients with early atherosclerosis. Smoking may further impair the response, implying that smoking has exaggerated response to sympathetic stimulation of conduit and resistance vessels. The abnormal response was abolished by pretreated administration of doxazosin, suggesting that the involved mechanisms are related to alpha(1)-adrenoceptors.     

Circadian Blood Pressure Rhythm in Primary and Secondary Hypertension

Circadian blood pressure variability was recorded in patients with primary hypertension and with different forms of secondary hypertension using ambulatory 24-h blood pressure measurement. A group of 20 patients with different forms of secondary hypertension was compared with a matched group of patients with primary hypertension. Although the mean 24-h blood pressure was not different between the two groups, the patients with secondary hypertension had significantly higher systolic blood pressure during sleep and higher systolic and diastolic blood pressure in the early morning, compared with the primary hypertension group. This nocturnal blood pressure fall was then investigated in various groups of patients with different forms of secondary hypertension and compared with normotensives and patients with primary hypertension. Patients with mild primary hypertension (n = 152) and with severe primary hypertension (n = 30) had the same blood pressure fall (14–16 mm Hg systolic and diastolic) during the night (23:OO–05:OO h) as normotensives (n = 20). However, in patients with renoparenchymal hypertension (n = 29), renovascular hypertension (n = 20), hyperaldosteronism (n = 6), and hyperthyroidism (n = 14), the nocturnal blood pressure fall was significantly (p < 0.01) reduced. One patient with coarctation ofthe aorta and nine patients with primary hyperparathyroidism and elevated blood pressure had a normal circadian blood pressure profile with a normal nocturnal blood pressure fall. The heart rate decrease during the night was equal in all patient groups. Ambulatory blood pressure measurement allows blood pressure recording under everyday conditions, including nighttime. In primary hypertension the blood pressure variability exhibits the same circadian variation as in normotension, showing a marked nocturnal fall. However, in different forms of secondary hypertension, blood pressure shows a blunted circadian curve. This could have important diagnostic and therapeutic implications.