Higher Plasma Norepinephrine Levels Research Articles

Fasting plasma caffeine level in cirrhotic patients: relation to plasma levels of catecholamines and renin activity.

Fasting plasma caffeine concentrations, plasma levels of catecholamines and plasma renin activity were measured in patients with cirrhosis and control patients without hepatic dysfunction. A careful dietary history showed no significant difference in caffeine consumption (mean +/- S.E.) among 46 cirrhotics (86 +/- 7 mg per day) vs. 34 control patients (91 +/- 8 mg per day). Fasting plasma caffeine concentrations, however, were significantly higher (7.68 +/- 1.42 micrograms per ml) in cirrhotics than in controls (1.01 +/- 0.20 micrograms per ml) (p less than 0.01). Fasting plasma caffeine concentrations in cirrhotics varied significantly with Child's criteria, namely Child's A patients (2.06 +/- 0.38 micrograms per ml); Child's B patients (6.92 +/- 1.86 micrograms per ml), and Child's C patients (17.70 +/- 3.65 micrograms per ml) (p less than 0.001). In 44 cirrhotics, fasting plasma caffeine concentrations were compared with plasma levels of catecholamines and plasma renin activity. Plasma epinephrine concentrations were normal; however, plasma norepinephrine concentrations were increased in six cirrhotics, and plasma renin activities were increased in 28 cirrhotics. After a 3-day caffeine abstinence, plasma caffeine concentration and renin activity were significantly decreased (p less than 0.01), and high plasma norepinephrine levels were also decreased in 12 cirrhotics. Plasma caffeine concentration, renin activity and norepinephrine level did not change in a control group of cirrhotics who continued to receive caffeine for 3 days (n = 6). After abstinence from caffeine, the decrease of fasting plasma caffeine concentration correlated well with the decrease of plasma renin activity (r = +0.746, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Sleep Deprivation in the Rat: IX. Recovery

Eight rats were subjected to total sleep deprivation, paradoxical sleep deprivation, or high amplitude sleep deprivation until they showed major deprivation-induced changes. Then they were allowed to sleep ad lib. Three rats that had shown the largest temperature declines died within two to six recovery days. During the first 15 days of ad lib sleep, surviving rats showed complete or almost complete reversal of the following deprivation-induced changes: debilitated appearance, lesions on the paws and tail, high energy expenditure, large decreases in peritoneal temperature, high plasma epinephrine and norepinephrine levels, and low thyroxine levels. The most prominent features of recovery sleep in all rats were immediate and large rebounds of paradoxical sleep to far above baseline levels, followed by lesser temporally extended rebounds. Rebounds of high amplitude non-rapid eye movement (NREM) sleep occurred only in some rats and were smaller and less immediate.

Role of stress in the exacerbation of chronic illness: Effects of clonidine administration on blood pressure and plasma norepinephrine, cortisol, growth hormone and prolactin concentrations

Systolic blood pressure (SBP), diastolic blood pressure (DBP), and plasma norepinephrine (NE), cortisol (CRT), growth hormone (GH) and prolactin (PRL) were studied before and after clonidine (2.5 μg/kg i.m.) administration in 193 chronic severely ill patients and 193 normal subjects matched by age and sex. During exacerbation periods (positive manifestations of impairment and progressive disease), the patients showed higher NE, CRT and DBP than the normals or when they were investigated during non-exacerbation periods (92 of the 193). Clonidine induced sharp, marked reductions of NE, CRT and DBP, plus a sudden increase of GH, in all the patients during exacerbation periods. Non-significant reductions of NE, CRT and DBP were observed in normals and in patients during non-exacerbation periods. On the other hand, the GH increase registered during exacerbation periods was of an order of magnitude higher than that registered in normals and in patients during non-exacerbation periods. Significant reduction of SBP was registered both in normals and patients (exacerbation and non-exacerbation periods). Some tendency to PRL lowering was observed during exacerbation periods only. A high positive correlation between NE and DBP (pre- and post-clonidine values) was obtained during exacerbation periods in patients, but not in normals or during non-exacerbation periods in the patients. Similarly, a close negative correlation was obtained between CRT and GH (postclonidine values) during exacerbation periods, but not in normals or during non-exacerbation periods. No significant correlation was found between NE and SBP in any group of subjects. The clonidine-induced changes in GH and CRT observed in the patients during exacerbation periods were in striking contrast to the absence of these changes in depressed patients. This finding is consistent with the low rate of depression (6.7%) registered among our patients during exacerbation periods. The high plasma NE and CRT levels registered in chronic severely ill patients during exacerbation periods reflect a central and peripheral sympathetic hyperactivity, accompanied by an overactivity of the pituitary — adrenocortical axis. The strong reduction of DBP, NE and CRT, along with the sharp and great increase of GH, might be useful as indicators in assessing the exacerbation and progression of severe chronic illnesses.

Pre-menopausal and post-menopausal depressed women.

In a consecutive series of 28 depressed women, pre-menopausal (n = 13) and post-menopausal (n = 15) patients were compared. Post-menopausal women had significantly higher levels of plasma norepinephrine, plasma 3-methoxy-4-hydroxyphenylglycol, post-dexamethasone plasma cortisol, cerebrospinal fluid 3-methoxy-4-hydroxyphenylglycol and corticotropin-releasing hormone. However, when biologic measures were adjusted for age by analyses of covariance there were no significant differences. Pre-menopausal women had had significantly more life events before the onset of depression than post-menopausal women. The implications of these findings are discussed.

Norepinephrine alterations under stress conditions following the regular practice of meditation.

The present study reexamined an investigation that found enhanced plasma norepinephrine (NE) levels during isometric handgrip after 30 days of meditation practice. Since hemodynamic activity did not show corresponding increases, it was suggested that meditation had down regulated the cardiovascular response to sympathetic stimulation. The present study assessed response to venipuncture as well as isometric stress. At posttest, meditators showed a trend towards higher plasma NE levels than controls during isometric handgrip. However, in contrast to previous speculation, this did not appear to represent cardiovascular down-regulation. At the same time, meditators produced the greater NE levels during venipuncture, accompanied by marginally lower heart rate. The results support the association between regular meditation and noradrenergic hyperactivation, but suggest the need for further investigation of underlying mechanisms.

Plasma norepinephrine level in affective disorders. Relationship to melancholia.

The plasma norepinephrine (NE) level was measured in 45 depressed patients and in 41 normal control subjects. Patients who met DSM-III criteria for a major depressive episode with melancholia (MDE-MEL; N = 16), and those with MDE but with melancholia in a previous episode (MDE-PMEL; N = 8), had significantly higher levels of plasma NE than normal control subjects while lying and standing and a greater change in the levels; whereas, patients with MDE alone (N = 10) and patients with dysthymic disorder (N = 11) had levels of NE comparable with control levels. Bipolar patients (N = 7), all with current melancholia or a history of it, had significantly lower levels of NE while lying down or standing than depressed unipolar patients with similar histories of melancholia. Among unipolar patients with melancholia, nonsuppressors on the dexamethasone suppression test had significantly higher lying-down NE values than did suppressors, suggesting that dysregulation of both the hypothalamic-pituitary-adrenal axis and the peripheral sympathetic nervous system occur together in this subgroup of depressed patients.

Treatment of Mild Hypertension With Progressive Muscle Relaxation

Effects of progressive muscle relaxation (PMR) and of attention control were investigated in a prospective randomized trial of borderline or mild hypertensive patients. Both groups received placebo and had the same number of clinic return visits. After 22 weeks the average mean home BP in PMR decreased 3 mm Hg, whereas in controls BP increased 2 mm Hg. Progressive muscle relaxation had no significant effect on the clinic BP. The response to PMR was not uniform. Responders were characterized by faster heart rates and higher plasma norepinephrine levels. The responders also showed a decrease of anxiety scores during the trial. Progressive muscle relaxation is a time-consuming procedure. Blood pressure responses do not substantially exceed the placebo effects in unselected patients. However, relaxation may be suitable for young, anxious patients with mild hypertension who have a high resting sympathetic tone.

Effects of intense exercise training on plasma catecholamines in coronary patients.

This paper reports the effect of 12 mo of intense endurance exercise training on the plasma catecholamine response to exercise in 11 male patients [aged 50 +/- 8 yr (mean +/- SD)] with coronary artery disease. A substantial adaptation to training was attained as evidenced by a 42% increase in maximum O2 uptake capacity. At rest, heart rate was lower after training, but resting blood pressure and plasma catecholamines were unchanged. At the same absolute work rate, plasma norepinephrine and epinephrine levels, rate pressure product, and ischemic S-T segment depression were all significantly lower after training. A higher plasma norepinephrine level was attained at maximal exercise after training (2,049 +/- 654 before vs. 3,408 +/- 1,454 pg/ml after, P less than 0.025); this was associated with a higher systolic blood pressure (175 +/- 25 before vs. 188 +/- 22 mmHg after, P less than 0.025) and a higher rate-pressure product (25.3 X 10(3) +/- 4.5 X 10(3) before vs. 27.6 X 10(3) +/- 5.2 X 10(3) after, P less than 0.025). Despite the higher plasma norepinephrine level and rate pressure product, S-T segment depression at maximal exercise was unchanged. These findings suggest that some patients with coronary arterial disease can attain a higher myocardial O2 requirement, without electrocardiographic evidence of increased ischemia, after prolonged strenuous exercise training.

High plasma norepinephrine levels in patients with major affective disorder

Lake, Raymond; Pickar, David; Zeigler, Michael; Lipper, Stephen; Slater, Stanley; Murphy, Dennis Author Information

High plasma norepinephrine levels in patients with major affective disorder.

The authors found that patients with major affective disorder had higher levels of plasma norepinephrine and higher pulse rates (tachycardia) than healthy control subjects, but their blood pressures were normal. These measurements were similar in all three subgroups of patients with affective disorder--manic, bipolar depressed, and unipolar. Because norepinephrine is the primary neurotransmitter of the sympathetic nervous system, these data suggest sympathetic hyperactivity in the major affective disorders. This conclusion is compatible with recent speculation based on the effect of antidepressants on noradrenergic receptors and a failure of alpha-receptors to downregulate normally in patients with major affective disorder.

Response of plasma norepinephrine and epinephrine to dynamic exercise in patients with congestive heart failure

The activity of the sympathetic nervous system is increased at rest in patients with congestive heart failure. To determine whether this augmentation is carried over during dynamic upright exercise, 14 patients with congestive heart failure were stressed maximally during upright bicycle ergometry. Plasma norepinephrine and epinephrine levels were measured in the basal upright (sitting) posture before and during maximal exercise. The results were compared with those in six healthy control subjects before and during maximal exercise. Plasma norepinephrine increased during exercise from a mean (± standard error of the mean) of 650 ± 95 to 1,721 ± pg/ml in the group with heart failure. This increase was significantly less (p < 0.001) than that in the control group (from 318 ± 36 to 3,230 ± 418 pg/ml). However, for equivalent levels of total body oxygen consumption (V̇O 2), the group with heart failure had higher levels of plasma norepinephrine than the control group. Plasma epinephrine was similar in the two groups in the basal upright position (92 ±18 and 92 ± 26 pg/ml), but it increased more during exercise in the normal subjects (743 ± 210 pg/ml) than in the group with heart failure (167 ± 67 pg/ml) (p < 0.001). The percent increase in norepinephrine correlated with the percent change in V̇O 2 in the group with heart failure (r = 0.62, p < 0.02), but the percent change in epinephrine did not. There is, therefore, a disturbance in the sympathetic nervous system during exercise in patients with congestive heart failure. Although norepinephrine increases in such patients to a greater extent than in normal subjects at lower levels of exercise, the extremely high levels of norepinephrine and epinephrine generated by normal subjects during maximal upright exercise do not occur in patients with heart failure.

The hyperactive child syndrome: Peripheral sympathetic nervous system function and the effect of d-amphetamine

We evaluated sympathetic nervous system function in medication-free hyperactive children by measuring plasma levels of norepinephrine (NE) and dopamine-β-hydroxylase and then comparing the effects of two therapeutic doses of d-amphetamine to placebo in these patients. The medication-free hyperactive patients and controls had similar plasma NE levels and blood pressures while recumbent, and similar increase in NE on standing, but the patients had a larger pressor response on standing. In the hyperactive patients d-amphetamine significantly increased blood pressure, pulse rate, and NE levels. The change in NE levels correlated with the change in amphetamine levels. The medication-free patients, when more anxious, had higher plasma NE levels.