Epinephrine Output Research Articles

Effect of chronic dietary treatment with L-tryptophan on the maintenance of hypertension in spontaneously hypertensive rats.

Chronic dietary administration of L-tryptophan at 2.5 and 5.0% by weight reduced the elevated systolic blood pressure of spontaneously hypertensive (SH) rats. Blood pressure was reduced significantly by 3 weeks after initiation of treatment and continued to fall during the course of the 15 weeks of treatment. Body weights of the treated rats were not affected significantly by treatment, nor were daily food and fluid intakes and urine outputs. SH rats, treated with the higher dose of tryptophan, also significantly reduced their urinary outputs of epinephrine and norepinephrine compared with SH controls, while both doses of tryptophan increased urinary outputs of dopamine significantly above that of SH controls. Treatment with tryptophan increased significantly the specific binding of [125I]angiotensin II (Ang II) to membranes from the diencephalon in a dose-dependent manner. Measurement of catecholamine concentration of the supernatant from homogenates used for the Ang II binding assay revealed a significant correlation between the specific binding of Ang II to brain membranes of the two tryptophan-treated groups and the concentration of norepinephrine in the supernatant. There was also a significant correlation between the specific binding of Ang II and the concentration of dopamine in the supernatant of the control group and the group treated with the higher dose of tryptophan. These results show that chronic dietary administration of tryptophan can reduce the elevated blood pressure of SH rats and support the possibility that this neutral amino acid may act via its effect on the concentration of the neurohormones, norepinephrine and dopamine, in the diencephalon to regulate the binding of Ang II to its receptors.

Direct evidence that an increase in aortic norepinephrine level in response to insulin-induced hypoglycemia is due to increased adrenal norepinephrine output.

This study reports on the major source of circulating norepinephrine that is known to increase, progressively, during sustained hypoglycemia induced by intravenous insulin administration. Plasma concentrations of epinephrine, norepinephrine, and dopamine were simultaneously determined for adrenal venous and aortic blood in dogs anesthetized with sodium pentobarbital. The model used allowed us to perform a functional adrenalectomy (ADRX), while continuously monitoring the adrenal medullary secretory function. Under basal conditions, the net output (micrograms/min) of adrenal epinephrine, norepinephrine, and dopamine were 0.169 +/- 0.074, 0.067 +/- 0.023, and 0.011 +/- 0.003, respectively. Plasma concentrations (ng/mL) of aortic epinephrine, norepinephrine, and dopamine were 0.132 +/- 0.047, 0.268 +/- 0.034, and 0.034 +/- 0.009. Following insulin injection (0.15 IU/kg, i.v.), the net output (micrograms/min) of adrenal epinephrine, norepinephrine, and dopamine increased gradually (p less than 0.05), reaching the values of 0.918 +/- 0.200, 0.365 +/- 0.058, and 0.034 +/- 0.007 30 min after insulin administration. Similarly, aortic epinephrine, norepinephrine, and dopamine concentrations (ng/mL) increased significantly (p less than 0.05) to 0.702 +/- 0.144, 0.526 +/- 0.093, and 0.066 +/- 0.024. The aortic glucose concentration (mg/dL) was diminished from 81.8 +/- 4.1 to 36.9 +/- 3.4 (p less than 0.01). After taking the blood sample at 30 min following insulin administration, ADRX was immediately performed. Five minutes after the onset of ADRX, the net output (micrograms/min) of adrenal epinephrine, norepinephrine, and dopamine increased further to 1.707 +/- 0.374 (p less than 0.05), 0.668 +/- 0.139 (p less than 0.05), and 0.052 +/- 0.017.(ABSTRACT TRUNCATED AT 250 WORDS)

Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

1. The output of corticotrophin releasing factor-like immunoreactivity (CRF) from the adrenal gland has been investigated using the 'adrenal clamp' technique in conscious calves. 2. Stimulation of the peripheral end of the splanchnic nerve for 10 min increased the mean output of CRF progressively, so that it had risen by about twentyfold, to a peak incremental value of 24 +/- 4 pmol min-1 kg-1 at 10 min. This response was significantly increased by stimulating in bursts at 40 Hz for 1 s at 10 s intervals, which raised the mean CRF output by 44 +/- 7 pmol min-1 kg-1 at 10 min (P less than 0.05). 3. The mean output of adrenaline and noradrenaline rose more abruptly in response to splanchnic nerve stimulation with peak incremental values realized within 2.5 min. However, the ratios of adrenal CRF to catecholamine output were closely similar during the later stages of stimulation (7.5-10 min). There was a similarly abrupt rise in adrenal cortisol output in response to splanchnic nerve stimulation which was, nevertheless, linearly related to arterial plasma ACTH concentration throughout. 4. In hypophysectomized calves, administration of adrenocorticotrophic hormone (ACTH1-24) at a dose of 5 ng min-1 kg-1 reduced the output of adrenal CRF in response to splanchnic nerve stimulation by about 50% (P less than 0.05). 5. CRF isolated from adrenal venous effluent plasma, collected both at rest and during splanchnic nerve stimulation, was separated by reverse-phase high-pressure liquid chromatography and found to elute in a position identical to that of human 41CRF. This suggests that adrenal CRF is structurally closely similar to its pituitary counterpart.

The adrenal contribution to the neuroendocrine responses to splanchnic nerve stimulation in conscious calves.

1. The extent to which the adrenal gland contributes to neuroendocrine responses to electrical stimulation of the peripheral end of the splanchnic nerve has been investigated in conscious calves in which the right nerve was stimulated either at 4 Hz continuously for 10 min or at 40 Hz in 1 s bursts at 10 s intervals for the same period. 2. It was confirmed that the release of neuropeptide Y (NPY) and of gastrin-releasing peptide (GRP) is potentiated by stimulation in bursts at a relatively high frequency and shown that the adrenal gland made a negligible contribution to these responses. 3. There was no detectable change in the concentration of vasoactive intestinal peptide (VIP) in the arterial plasma but the existence of a very small but highly significant rise in the output of VIP from the adrenal provided evidence that it was released within the gland in response to splanchnic nerve stimulation. 4. The concentration of calcitonin gene-related peptide (CGRP) in the arterial and adrenal venous effluent plasma was consistently below the level of detection of the assay. 5. Splanchnic nerve stimulation resulted in an abrupt rise in the output of both free and total met5-enkephalin-like immunoreactivity from the adrenal gland which was substantially potentiated by stimulating in bursts. This pattern of stimulation also increased the proportion released in a high-molecular-weight form. 6. Stimulation in bursts significantly enhanced the output of both adrenaline and noradrenaline from the adrenal and resulted in the release of proportionately more noradrenaline. Small amounts of dopamine and DOPAC were also released during splanchnic nerve stimulation and the output of dopamine was significantly increased by stimulating in bursts. 7. Both patterns of stimulation elicited an abrupt rise in mean plasma adrenocorticotrophic hormone (ACTH) concentration, which was associated with an increase in mean adrenal cortisol output and the former effect was significantly enhanced by stimulating in bursts. 8. It is concluded that certain responses to splanchnic nerve stimulation are significantly potentiated by an intermittent high-frequency pattern of stimulation, including all those that are attributable to adrenal medullary activity, whereas others are apparently unaffected by changes in stimulus pattern.

Effects of Lidocaine Infusion on the Sympathetic Response to Abdominal Surgery

Activation of afferent nerves in the area of surgery is a cause for surgical pain and stress. Intravenous (IV) lidocaine has been shown to inhibit postoperative pain. In the present double-blind study, the effects of a continuous IV infusion of lidocaine (2 mg/min) on the sympathoadrenal stress response to surgery were evaluated in 38 patients scheduled for elective cholecystectomy who were randomly assigned to two groups. In one group, lidocaine infusion was started 30 min before the operation and continued for 24 hr after surgery (n = 18). In the second group (n = 20), saline was infused. The increases in heart rate and blood pressure after tracheal intubation were not significantly different between the groups, but tachycardia and hypertension associated with extubation was prevented in patients given lidocaine. Differences in blood pressure and heart rate between the two groups were otherwise not significant intra- or postoperatively, nor were differences in blood glucose or plasma catecholamine concentrations during the first 24 hr after skin incision. Urinary catecholamine concentrations did not differ significantly in the two groups during the first postoperative day, but during the second postoperative day urinary output of epinephrine and norepinephrine were significantly less in the group of patients receiving lidocaine infusion. It was concluded that the IV infusion of lidocaine during and after major abdominal surgery suppresses extubation-induced hypertension and tachycardia but does not inhibit the general sympathetic response during the first postoperative day. However, lidocaine infusion reduces urinary output of catecholamines during the second postoperative day, suggesting a more rapid decline in the sympathoadrenal response postoperatively in the experimental group.

Muscarinic and nicotinic mechanisms in the responses of the adrenal medulla of the dog and cat to reflex stimuli and to cholinomimetic drugs.

In isolated perfused adrenal glands of the cat, muscarinic and nicotinic agonists selectively released adrenaline and noradrenaline respectively. In isolated perfused adrenal glands of the dog, the output of adrenaline and noradrenaline remained in a fixed ratio at rest and when stimulated by muscarinic or by nicotinic agonists. In the anaesthetized dog, a combination of muscarinic and nicotinic antagonists was needed to block reflex responses of the adrenal medulla. A nicotinic antagonist was more effective in blocking the baroreceptor reflex response than the chemoreceptor reflex response.

Increases in blood flow from the adrenal gland following medial hypothalamic stimulation in the cat

Medial hypothalamic sites previously shown to elicit either flight or defense were stimulated in the anesthetized cat. The rate of blood flow from the adrenolumbar (AL) vein ipsilateral to the side of stimulation was measured, as well as the adrenal output of norepinephrine and epinephrine (E). Stimulation at nearly 15% of the hypothalamic sites increased ipsilateral AL venous flow more than 20% over baseline rates. These sites also significantly increased heart rate, mean arterial pressure, and output of E from the ipsilateral adrenal gland. These observations suggest that hypothalamic sites where stimulation increased AL venous flow may overlap with regions that selectively mediate the release of E from the adrenal medulla.

Bereavement and catecholamines

Urinary catecholamine output was studied in 59 middle-aged and elderly persons who were either acutely bereaved ( n=39) or threatened with the loss of a spouse ( n=20). The study was done with the hypothesis that urinary catecholamine output would be elevated among the bereaved subjects both in comparison to norms in the literature for non-stressed controls and to the group of subjects who were threatened with a loss. It was also expected that individually high measures of psychological distress would be associated with high urinary catecholamines. Twenty-four hour urinary output of norepinephrine and epinephrine was observed to be higher than normal during acute bereavement but was not associated with depression scores. No differences were found between those who had experienced an actual loss two months earlier and those who were threatened with a loss. Expected relationships between indices of psychological distress and catecholamine output were not observed. Finally, an association was found between increasing age and higher levels of urinary norepinephrine and epinephrine output among acutely bereaved subjects, suggesting that the adaptation of the sympathetic-adrenal medullary system to stress among older persons is slower.

Catecholamine excretion and beta-adrenergic responsiveness in estrogen-treated rats.

Chronic treatment with an estrogenic agent is known to reduce the responsiveness to beta-adrenergic stimulation in rats. To assess the possibility that endogenously produced catecholamines may play a role in this phenomenon, female rats were treated either with implanted Silastic tubes containing estradiol benzoate (26 micrograms/kg/day) or with empty tubes. After 12 weeks of treatment, the dipsogenic, colonic temperature and tail skin temperature responses to acute administration of the beta-adrenoceptor agonist, isoproterenol, were blunted compared to controls. Each of these responses was negatively correlated with serum estradiol concentration measured by radioimmunoassay. Urinary norepinephrine output was elevated significantly in treated rats during a 24-hour basal period. During a 2-hour exposure to air at 4 degrees C, urinary outputs of norepinephrine, epinephrine, and dopamine were elevated significantly above those of controls. There were significant positive correlations between plasma estradiol concentration and the outputs of each of the above catecholamines during the 24-hour basal period and during cold exposure, with norepinephrine being the most strongly correlated. Dipsogenic and metabolic (tail skin and colonic temperature) responses to administration of isoproterenol were negatively correlated with catecholamine excretion during both the basal 24-hour period and during cold exposure. These results suggest that reduced beta-adrenergic responsiveness in estrogen-treated rats may have resulted from down-regulation of beta-adrenoceptors associated with increased secretion of catecholamines induced by chronic estrogen treatment.

Substance P given intrathecally at the spinal T9 level increases adrenal output of adrenaline and noradrenaline in the rat

Administration of 10 μg of substance P intrathecally to the spinal T 9 level of the adult rat. anaesthetized with urethane, provoked an increase in free catecholamines in plasma taken from the inferior vena cava. Adrenaline levels at l min after administration were154.8 ± 10.8% (mean±SE;n = 11) of preadministration levels and noradrenaline levels were153.5 ± 11.8% of preadministration levels. Differences between the values of free catecholamines in animals given substance P vs those given vehicle only were statistically significant at 1 and 10 min postinjection, but not at 30 min. Administration of a substance P analogue with central antagonistic properties 15 min before substance P was given prevented expression of the effects of substance P. These results suggest that substance P may be an excitatory chemical mediator of synaptic transmission in spinal pathways controlling adrenal medullary output. Thus dysfunction of substance P mechanisms may underlie some animal models of hypertension and may be involved in some cases of essential hypertension in man as well as in autonomie dysfunction associated with some neurological entities.

Behavioural and endocrine reactions in boys scoring high on Sennton neurotic scale viewing an exciting and partly violent movie and the importance of social support

Psychoendocrine and behavioural effects elicited by viewing an exciting and partly violent movie were studied in 12-year-old boys ( n = 42). The boys were divided into three groups. Group A ( n = 13) consisted of boys scoring below the median value on the Sennton neurotic scale for vegetative anxiety symptoms. Group B ( n = 13) consisted of boys scoring above the median value on the Sennton neurotic scale. None of these boys had ever visited a psychiatric treatment centre, and they all came from the same school. A third group, Group C ( n = 16), consisted of boys who, at least once, had visited an out-patient clinic at a child psychiatric treatment centre for neurotic problems. These boys attended different schools in the hospital catchment area. Group C had the same mean score on the Sennton neurotic scale as did Group B. By having two groups of boys scoring both high on the Sennton neurotic scale, one of which knew the other boys and one that did not, we were able to study possible effects of social support on psychobiologic reactions in neurotic boys. The boys' reactions to the movie were assessed by: (1) self-ratings; (2) direct observations of the boys by a team of trained child psychologists; and (3) by analysis of urinary output of adrenaline, noradrenaline and cortisol. Group B rated their experience the strongest, viewing the movie, while Groups A and C rated themselves as rather unaffected by it. Group C was rated less verbally active, both during the control and the film periods, than were the other two groups. Group A was most motorically active during the film period. There were no significant differences during the control period in endocrine variables. During the film period Group C excerted significantly more noradrenaline than did Group A, and significantly more noradrenaline than did Group B. Intra-group differences in response to the movie were also assessed. Adrenaline excretion increased significantly only in Group C during the movie, compared with the control period. Furthermore, excretion of noradrenaline decreased significantly during the film period in Groups A and B. The A and B groups preferred to review scenes representing danger, while Group C preferred scenes representing security. It is suggested that psychosocial factors, e.g. novelty to the environment and lack of friends, caused the differences between Group C and the other two groups. Group C, which scored the same as Group B on Sennton neurotic scale, did not have access to social support in the form of friends during the movie. They were left alone with their anxiety, with little ability to express it in a group of unknown boys. Group B appeared to have coped in a more ‘open way’, expressing their emotions during the film period, possibly explaining this group's lower level of physiological arousal. The psychological vulnerability in Group C is further stressed by this group's desire to review scenes depicting security. It suggested that access to social support, here operationally defined as being together with friends, is an important intervening variable in predicting psychobiological effects of viewing exciting and violent motion pictures.

The relationship between circulating catecholamines and ST waveform in the fetal lamb electrocardiogram during hypoxia

Previous studies from this laboratory have shown that changes in the ST waveform in the fetal electrocardiogram are a sign of fetal asphyxia. In the present study, seven chronically instrumented fetal lambs between 117 and 143 days' gestation were studied during 16 one-hour periods of maternally induced hypoxia. The aim was to test the hypothesis of a relationship between the concentration of circulating catecholamines and T-wave amplitude. The response to hypoxia was age-dependent. Fetuses below 126 days of gestation did not react with electrocardiographic changes and output of epinephrine unless acidosis occurred. In more mature fetuses, hypoxia per se would induce a surge of epinephrine and changes in the ST waveform. Overall there was a strong correlation between the T/QRS ratio and the level of circulating epinephrine. During normoxia, epinephrine was undetectable (<0.1 nmol/L) in most fetuses; norepinephrine showed an increase at term. The analysis showed one fetus with chronic changes in the ST waveform (T/QRS ratio >0.30) related to a marked increase in the plasma level of epinephrine in spite of normal blood gas values. These findings complement previous results in the acute and chronically instrumented fetal lamb and suggest that changes in the ST waveform expressed as T/QRS ratio identify a change to anaerobic myocardial metabolism mediated by β-adrenergic stimulation.

Renal dysfunction as a possible cause of essential hypertension in predisposed subjects

In 65 young normotensive subjects with two hypertensive parents (HP), and in 55 matched subjects with two normotensive parents (NP), the following factors were measured: renal plasma flow (RPF), glomerular filtration rate (GFR) both as Inutest and creatinine clearances; 24-hr urinary output; plasma renin activity (PRA); Na and K in plasma and in 24-hr urine and 24-hr urinary excretion of aldosterone. In 30 HP and in 34 NP, the cardiac output and plasma concentrations of noradrenaline, adrenaline, and dopamine were also measured in the supine position and after 10 min of standing. The HP have greater RPF (P less than 0.01), faster GFR (P less than 0.02), greater 24-hr urinary output (P less than 0.05), and lower PRA (P less than 0.01) than the NP. All the other factors were similar in the two groups of patients. It is proposed that the differences in renal function in the HP and the NP may be due to an abnormality in tubular handling of ions and water in the HP, which may be responsible for the increase in blood pressure in a proportion of patients with essential hypertension.

Adrenal catecholamine output in response to stimulation of the splanchnic nerve in bursts in the conscious calf.

1. Different patterns of stimulation have been applied to the peripheral end of the right splanchnic nerve, below behavioural threshold, in conscious 2-5 week-old calves. 2. The effects of continuous stimulation at 4 Hz for 10 min were compared with those of stimulation at 40 Hz in 1 s bursts at 10 s intervals for the same period. Delivering the same total number of impulses in the form of bursts in this way increased the output of both adrenaline and noradrenaline and this increase was statistically significant in the case of adrenaline (P less than 0.02) but not noradrenaline. 3. The effects of stimulation in 1 s bursts at 10 s intervals for 2-3 min were investigated over the frequency range 10-150 Hz and compared with the effects of continuous stimulation over the range 1-15 Hz obtained previously in conscious calves of the same age (Edwards, Furness and Halle, 1980). The output of adrenaline but not noradrenaline was found to significantly greater in response to stimulation in bursts at frequencies of up to 40 Hz than when the equivalent number of impulses were delivered at a constant rate (P less than 0.02). 4. It is concluded that the release of catecholamines from the adrenal gland is maximal at relatively high frequencies (40-100 Hz) when the impulses are delivered in bursts.

The need for Power, sympathetic activation, and illness

This paper provides a brief summary of a number of recent research reports indicating thatn Power, if it is inhibited or stressed, is associated with high blood pressure and with the frequency and severity of infectious diseases. Other motive/stress or inhibition combinations failed to show these relationships. Blockedn Power apparently leads to chronic sympathetic activation, which, over time, results in high blood pressure and which increases epinephrine output that interferes with lymphocyte function, weakening the body's immune defenses against infectious diseases. On the other hand,n Power that is expressed successfully and rewarded may lead to better adaptation.

Catecholamine and cortisol excretion patterns in three-year-old children and their parents.

Urinary catecholamine and cortisol excretion was studied in a group of three-year-olds, their mothers and fathers during night rest, one day at home and one day at hospital. The stay in the hospital, which was part of a longitudinal study of the families, induced a pronounced rise in adrenaline excretion and a moderate increase in noradrenaline excretion in relation to the at-home level. Although the catecholamine excretion in relation to body weight was much higher in the children, the magnitude of the increase at the hospital was about the same in all the family members. The adrenaline excretion was also affected by the diverse conditions at the hospital and showed, for example, a marked decrease during lunch hour. The cortisol excretion at the hospital tended to be elevated only in fathers. On the average, mothers excreted about the same amount of adrenaline as the fathers at the hospital, but significantly more noradrenaline. In earlier studies males have shown a greater adrenaline output than females during achievement-demanding situations. The findings of this study were interpreted within the context of the specific challenge that the situation represented to the mothers. The mothers also excreted more noradrenaline in the at-home condition. Catecholamine and cortisol excretion levels within family members tended to be positively correlated, but the correlations were generally low.

Effect of Manual Lymphdrainage Massage on Blood Components and Urinary Neurogormones in Chronic Lymphedema

In an earlier paper we have shown that manual lymph drainage massage of edematous limbs can result in the excretion of up to 1 liter urine derived from reabsorption and transport from the interstitial fluid, simultaneously with significant changes in the excretion of urinary neurohormones. These findings indicated that histamine and serotonin were released from the edematous tissue and that circulation improved through increased output of adrenaline and noradrenaline. The results achieved led us to assume that similar changes may have occurred in the blood during treatment, and induced us to study the effect of manual lymphdrainage on various blood constituents and urinary neurohormones.

Adrenal medullary responses to stimulation of the splanchnic nerve in the conscious calf.

1. Right adrenal medullary and various cardiovascular responses to stimulation of the peripheral end of the right splanchnic nerve have been investigated in conscious calves, 2--5 weeks after birth. 2. The output of both adrenaline and noradrenaline was linearly related to stimulus frequency over the range 2.0--10.0 Hz, 2 1/2 min after stimulation was initiated. Peak outputs of both amines were obtained in response to stimulation at 15.0 Hz. 3. The output of adrenaline invariably exceeded that of noradrenaline, roughly in the proportion 3:2. At all frequencies tested between 7.0 and 40.0 Hz this difference was statistically significant (P less than 0.1). 4. Continuous stimulation at either 4.0 or 10.0 Hz produced a small but significant rise in the output of dopamine-beta-monooxygenase (DBH) activity from the right adrenal gland. Mean maximal outputs were obtained after 10 min; the levels were closely similar at both 4.0 and 10.0 Hz and could not be related to stimulus frequency or to the output of either adrenaline or noradrenaline. 5. The results are discussed in relation to perfusion studies in vitro and experiments in anaesthetized animals. It is concluded that the levels of DBH in adrenal effluent plasma is an unreliable index of catecholamine exocytosis in the conscious calf.

Effect of Food Deprivation (Fasting) on Plasma Gastrin Levels in Man

We studied plasma gastrin levels in 12 healthy men before and after 4, 8 and 10 days of total food deprivation. The gastrin levels during the starvation period were significantly lower than the preexposure values. No such changes were observed in 6 other men, serving as controls, who were allowed to eat ad libitum during the experiment. Blood glucose levels and urinary output of catecholamines were measured concurrently. A pronounced hypoglycemia and a doubting of the urinary output of adrenaline were observed during the fasting period. Thus, depression of plasma gastrin concentrations occurs during starvation despite the presence of some potent gastrin-releasing factors, such as hypoglycemia and increased release of adrenaline. It is suggested that these depressions could be due to the absence of another potent stimulator of gastrin release, namely food in the stomach, or to neurogenic inhibition of gastrin release secondary to a stress-induced elevation of the sympathetic tone.

Urinary excretion of adrenaline, noradrenaline, 17-OHCS, 5-hydroxytryptamine and certain electrolytes in 24-hour shift workers taking a 4-hour night nap.

Urinary excretion of adrenaline, noradrenaline, 17-OHCS, 5-hydroxytryptamine and certain electrolytes was measured in 15 male guards engaged in 24-hour shift work containing a 4-hour night nap. In the night nap, it was found that the urinary output of adrenaline had a significant negative correlation to a self-rated value of feeling about depth of sleep. Based on this finding, it is considered that adrenaline output may be useful as a sleep index. The urinary level of adrenaline during the night nap was as low as the level during usual normal night sleep. However, the level of adrenaline during a daytime nap after the night work was considerably high compared to those in the night nap and in the normal night sleep. This suggests that the daytime nap was possibly not so deep as night sleep.