Urinary Epinephrine Levels Research Articles

Urinary catecholamines, plasma renin activity and blood pressure in newborns: effects of narcotic withdrawal.

Blood pressure and plasma renin activity were studied in 13 infants of drug-dependent mothers (heroin and/or methadone) and 20 control newborns for a period of 21 days. Urinary excretion of epinephrine and norepinephrine were also measured at 24 and 48 h of age. The systolic blood pressure was found to be significantly elevated in newborns of drug-dependent mothers compared with controls (p less than 0.01), but diastolic blood pressure levels were similar. Plasma renin activity was significantly elevated (p less than 0.001) at 48-72 h and urinary epinephrine levels were significantly lower (p less than 0.05) at 24-48 h of age in the drug group, and norepinephrine levels were equivalent. Systolic hypertension and elevated plasma renin activity in these newborns of dependent mothers may be due to increased beta-adrenergic receptor sensitivity.

A Prospective Study of Corticosteroid and Catecholamine Levels in Relation to Viral Respiratory Illness

Urinary 17-OHCS, epinephrine and norepinephrine levels were studied for one week before and one week after the onset of acute, severe Adenovirus 4 respiratory illness in 12 Army recruits during Basic Combat Training. During the pre-illness period, a tendency was frequently noted for all three hormone levels to show "spiking" elevations two to four days before illness onset. There was also a tendency for 17-OHCS levels to rise on the day before fever onset. The possible relationship of these pre-illness hormonal changes to stressful experiences and, in turn, to altered host resistance to infectious illness is discussed. Following onset of respiratory illness, 17-OHCS, epinephrine and norepinephrine levels all showed about 60 percent increases over the early pre-illness period baseline value. Elevations of these hormones persisted for about four to five days, roughly in correlation with fever duration, with only slight differences in configuration and timing of curves from one hormone to the next. The problem of evaluating which of several independent variables operating concurrently during infectious illness may be responsible for stimulating the final common neuroendocrine pathways is discussed.

Toward a biochemical classification of depressive disorders. I. Differences in urinary excretion of MHPG and other catecholamine metabolites in clinically defined subtypes of depressions.

The urinary excretion of 3-methoxy-4-hydroxyphenylglycol (MHPG) and other catecholamine metabolites was measured in a series of 63 patients with various clinically defined subtypes of depressive disorders. MHPG excretion was significantly lower in patients with bipolar manic-depressive depressions and schizo-affective depressions than in patients with unipolar nonendogenous depressions. Patients with schizophrenia-related depressions also excreted reduced levels of MHPG when compared with patients with unipolar nonendogenous depressions. Moreover, levels of urinary epinephrine and metanephrine were significantly lower in patients with schizophrenia-related depressions. These data, coupled with our recent finding that patients with schizophrenia-related depressions had significantly higher levels of platelet monoamine oxidase activity than control subjects of patients with unipolar endogenous depressions, suggest that we can discriminate three biochemically discrete subgroups of depressive disorders corresponding to the following clinically defined subtypes: (1) the bipolar manic-depressive depressions plus the schizo-affective depressions; (2) the unipolar nonendogenous depressions; and (3) the schizophrenia-related depressions.

Choline administration to the rat increases urinary catecholamines.

Previous studies have shown that choline administration accelerates the synthesis of acetylcholine (ACh) in rats and raises ACh levels in brain, adrenal medulla, and other tissues receiving a cholinergic innervation. After 24 hours, this precursor-induced elevation in ACh levels causes tyrosine hydroxylase activity to increase, unless the adrenals have been previously denervated. We now report that oral choline administration also increases urinary epinephrine levels, probably by enhancing the release of the catecholamine from the adrenal gland. For four consecutive 4-day periods, male Sprague-Dawley rats received (1) no treatment, (2) water, (3) choline (20 mmoles/kg), and (4) water, and excreted 157, 200, 646, and 267 ng of epinephrine per 24-hour period, respectively. Urinary norepinephrine levels also increased on days that the animals received choline. Choline failed to increase urinary epinephrine levels among rats previously subjected to bilateral adrenal denervation; in contrast, nicotine, a direct-acting cholinergic agonist, continued to elicit this increase. Thus, choline administration apparently potentiates the increase in urinary epinephrine produced by treatments that accelerate the flow of impulses along the splanchnic nerves. These data provide additional support for the hypothesis that choline administration, by increasing presynaptic ACh levels, enhances cholinergic transmission at preganglionic synapses of the sympathetic nervous system.

Catecholamines metabolism in thyroid diseases. I. Epinephrine secretion rate in hyperthyroidism and hypothyroidism.

We have measured the secretion rate of epinephrine in 6 euthyroid, 6 hyperthyroid, and 6 hypothyroid subjects infused at a constant rate for a one hour period with tritiated epinephrine (.01 muc/kg/min) (New England Nuclear Inc.). Plasma and urinary levels of epinephrine were measured by modifying the fluorometric method of Anton and Sayre. Plasma levels of epinephrine were 3.0 +/- 3.0 ng/100 ml (mean +/- SD) in normal subjects, compared to 4.4 +/- 3.5 ng/100 ml (mean +/- SD) in hyperthyroid subjects. In urine, epinephrine values ranged from 1.3 mug/day to 6.1 mug/day in normal subjects. Mean value observed in hyperthyroidism was 4.9 +/- 2.6 mug/day and 3.8 +/- 1.0 mu/day in hypothyroidism. Plasma secretion rates averaged 48 +/- 27 mug/kg/day in normal subjects, compared to 54 +/- 18 mu/kg/day in hyperthyroidism and 43 +/- 20 mug/kg/day in hypothyroidism. Likewise, the mean urinary secretion rate was 55 +/- 27 mug/kg/day in normal subjects compared to 60 +/- 22 mug/kg/day in hyperthyroidism and 50 +/- 28 mug/kg/day in hypothyroidism. There is no statistical difference between the values found in the three groups of subjects (plasma and urine). Therefore, these results would indicate that the signs and symptoms encountered in hyperthyroidism are not secondary to a high secretion rate of epinephrine.

Urinary epinephrine and norepinephrine levels in women athletes during training and competition.

Training and competitive epinephrine and norepinephrine levels and proportions were compared in two groups of women athletes to determine whether changes in catecholamine excretion reflect the added mental stress of athletic competition on physical effort. An intercollegiate basketball team and a group of track and field athletes volunteered as subjects. Competitive epinephrine urinary levels were significantly (P less than 0.01) higher than training levels. A concomitant rise in the norepinephrine with an increase in physical effort was observed in both groups of athletes following training sessions as well as after athletic competition. Track and field athletes trying to qualify for an international team exhibited significantly ( less than 0.01) higher epinephrine levels than the team members; thus suggesting that anticipation of competition imposes a mental stress on an athlete. Constant changes in the catecholamine pattern as against a normal work load have yet to be established.

Secretion of Anterior Pituitary Hormones in Man: Effects of Ethyl Alcohol

The possibility that previously described effects of ethyl alcohol on peripheral endocrine glands might be mediated via pituitary prompted this investigation on the effects of ethanol on anterior pituitary secretion. Nine healthy male subjects were given beverage containing ethanol (1.5 g/kg) or beverage alone per os in a randomized cross-over study and plasma ACTH, FSH, GH, LH and TSH were measured by specific radioimmunoassays up to 15 h and the urinary levels of adrenaline and noradrenaline by fluorometry. A combined LRF and TRF test was also carried out in similar series of experiments. During the whole experiment there were no significant differences in the plasma levels of ACTH, FSH and TSH or in the urinary levels of adrenaline and noradrenaline between ethanol treated and control subjects. Plasma FSH, LH and TSH responses to LRF and TRF stimulation were also similar in alcohol treated and control subjects. Plasma ACTH values were high (113-270 pg/ml) both in control and ethanol experiment suggesting that the subjects experienced apprehension toward the experiment. Plasma GH level exhibited a non-sleep related burst in the late evening (from 0.4 ng/ml at 6 p.m. to 3.1 ng/ml at 10 p.m., p less than 0.01). This increase was not seen after alcohol ingestion (p less than 0.01). Plasma LH levels were significantly lower after 6 and 13 h in alcohol treated subjects than in controls (65 vs. 106 ng/ml, p less than 0.01 and 74 vs. 121 ng/ml, p less than 0.05 respectively). Because ethanol had no effect on the resting level of plasma GH or on the LH response to LRF, WE SUggest that ethanol exerts these effects on a suprapituitary site.

The effect of visual sexual stimulation on urinary excretion of adrenaline and noradrenaline in impotent patients.

In 15 impotent patients, the effect of visual sexual stimulation was evaluated by measuring their urinary levels of adrenaline and noradrenaline, before and after stimulation. Both adrenaline and noradrenaline increased in the urine over the base levels in response to the visual sexual stimulation. The average increases were 1.5 times for adrenaline, and 1.4 times for noradrenaline. There was an evident correlation between the degree of sexual excitation and the excretion of adrenaline and noradrenaline into urine.

Urinary epinephrine and norepinephrine responses to chair restraint in the monkey

Mean urinary epinephrine levels show a greater than three-fold increase (8.2 μg/day versus baseline of 2.2 μg/day) in monkeys during the first three days after placement in a restraining chair. Epinephrine levels remain significantly elevated, however, only during the first week in a total eight-week period of restraint. Although there also was a tendency for slight initial increases in urinary norepinephrine levels to occur, the changes were not statistically significant. There were no significant differences in either epinephrine or norepinephrine levels in monkeys during cage housing as compared to the second month of chair restraint, indicating no sustained effects of chair restraint on the sympathetic-adrenal medullary system over a two-month period. Some practical, methodological implications of the findings are discussed.

Catecholamines and indoleamines in patients with Duchenne muscular dystrophy.

Several studies have raised the question of abnormal biogenic amine metabolism in Duchenne muscular dystrophy (DMD). A small group of DMD patients and controls were screened for abnormalities in systemic biogenic amine metabolism in a carefully controlled clinical environment The mean 24-hour urinary excretion levels of norepinephrine, epinephrine, and 5-hydroxyindoleacetic acid (5-HIAA) were identical in the group of DMD patients compared to their normal sibling controls. In the cerebrospinal fluid (CSF), 5-HIAA and homovanillic acid (HVA) levels were similar in DMD patients and controls, and no 5-hydroxytryptamine (5-HT) was detected in the CSF of either group. This study suggests that the characteristic lesions of DMD do not result from a simple excess of circulating amines.

Patterns of endocrine reactivity in patients with recent myocardial infarction. Clinical and biochemical correlations: trial of endocrine therapy.

The following endocrine function parameters were studied serially in a group of 10 patients with recent myocardial infarction: blood and urinary levels of epinephrine and norepinephrine, urinary excretion of vanillyl-mandelic acid; protein-bound iodine, Hamolsky test (Hamolsky, Stein, and Freedberg, 1957); blood insulin; 24-hour urinary excretion of 17-hydroxycorticoids, sodium, and potassium. The acute phase of myocardial infarction, especially in those patients with a severe clinical course (rhythm disturbances, coronary insufficiency, circulatory failure), was associated with disturbed endocrine reactivity. The most frequent and the earliest feature was the increased level of the 24-hour urinary excretion of epinephrine, combined with a pronounced decrease in blood insulin level. Later in the course of the disease, as the adrenergic reactivity returned to normal, there was an increase in blood insulin to normal levels. In 3 patients with severe clinical symptoms of acute myocardial infarction, there were, in addition to the increased 24-hour urinary excretion of catecholamines, a decreased blood insulin, higher than normal levels of protein-bound iodine, and of the Hamolsky test. One of these patients developed hypoadrenia. It is possible that the abnormal endocrine reactions accelerate the catabolic processes within cardiac tissue (catecholamines, thyroid hormones), especially when there is a possible functional deficiency of hormones, occurring as a general adaptation reaction to stress (cortisol, insulin). The disturbances that follow may be dangerous for the patient.

Urinary epinephrine and norepinephrine responses to 72-hr. avoidance sessions in the monkey.

Marked elevations in urinary epinephrine levels occur in response to 72-hr. conditioned avoidance sessions in the monkey. The response is relatively rapid and brief, reaching a peak on the first avoidance day, declining on the second and third avoidance days, and returning to baseline levels immediately on the first recovery day. In some instances epinephrine levels fell substantially below baseline values during the recovery period. Smaller but significant elevations in urinary norepinephrine levels occur during the avoidance session, with considerably larger elevations often ensuing for many days in the recovery period-a response phase apparently not previously reported. These epinephrine and norepinephrine changes, while substantial, do not appear to represent maximal sympathetic-adrenal medullary responses nor was any evidence of exhaustion of this system observed. Repetition of the 72-hr. avoidance experience is associated generally with both diminishing basal urinary catecholamine levels and urinary catecholamine response to avoidance. Significant responses persisted, however, through at least six successive sessions at monthly intervals. Substantial individual differences were observed between monkeys with respect to mean urinary epinephrine and norepinephrine response to avoidance.

Rehabilitation of the patient with acute myocardial infarction

Rehabilitation of the patient with acute myocardial infarction

Effect of alcohol on ex-creation of catechol amines in conditions givings rise to anxiety.

An investigation was made of the effect of alcohol on the concentration of adrenaline and noradrenaline in the urine and on blood pressure and heart rate of men who were learning to fly a glider. It was shown that the noradrenaline concentration was elevated during the period of flight and that alcohol prevented this increase. No changes were demonstrated in the urinary adrenaline levels, blood pressure or pulse rate recordings. Submitted on February 20, 1958