Biomedical subjects

E H Mougey

Publications and source records attributed to E H Mougey.

At least 19 recordsLinked to original sources

PubMed2000

Chronic sustained stress increases levels of anterior pituitary prolactin mRNA.

Our laboratory is investigating the effects of chronic stress on physiological, endocrine and behavioral measures, in order to elucidate the neuronal substrates for the pathophysiological consequences of stress in humans. In these studies, we have employed a rodent model of sustained stress in which rats are exposed to around-the-clock intermittent footshock that can be avoided or escaped by rats in the controllable stress group, but not by rats in the uncontrollable stress group. Each rat in the uncontrollable stress group is paired (yoked) to a rat in the controllable stress group such that the controllable stress group rat avoids or escapes shock for both rats. A third group of rats receives no shock (controls). We have previously reported that in male rats, plasma prolactin levels were elevated after 3 days of stress in both stress groups. In the present experiments we determined whether the increases in plasma prolactin were correlated with increases in anterior pituitary prolactin mRNA. In addition, we measured hormones and mRNA at three time points and we examined these responses in female as well as male rats. Adult male and female Sprague-Dawley rats were exposed to chronic stress for 1, 3 or 14 days. In unstressed control rats, levels of anterior pituitary prolactin mRNA were fivefold higher in female as compared to male rats. However, stress increased levels of anterior pituitary prolactin mRNA over baseline in both genders. After 1 day of stress, anterior pituitary prolactin mRNA levels increased in male and female rats belonging to both stress groups, with no significant difference seen between the uncontrollable vs. controllable stress groups. After 3 days of stress, anterior pituitary prolactin mRNA levels were even more elevated, and rats in the uncontrollable stress group had higher anterior pituitary prolactin mRNA levels than those in the controllable stress group. After 14 days of stress, there were no significant differences in control and stressed groups with respect to anterior pituitary prolactin mRNA. These data suggest that chronic sustained stress increases the synthesis of anterior pituitary prolactin mRNA during the first days of stress, and that levels return to prestress values sometime between 3 and 14 days of stress.

Adrenocorticotropic Hormone↗

PubMed2000

Treadmill exercise training blunts suppression of splenic natural killer cell cytolysis after footshock.

This study extended to treadmill exercise training our prior report (Dishman RK, Warren JM, Youngstedt SD, Yoo H, Bunnell BN, Mougey EH, Meyerhoff JL, Jaso-Friedmann L, and Evans DL. J Appl Physiol 78: 1547-1554, 1995) that activity wheel running abolished the suppression of footshock-induced natural killer (NK) cell cytolysis. Twenty-four male Fischer 344 rats were assigned to one of three groups (n = 8, all groups): 1) a home-cage control group, 2) a sedentary treatment group, or 3) a treadmill-running group (0 degrees incline, 25 m/min, 35 min/day, 6 days/wk). After 6 wk, the treadmill and sedentary groups received 2 days of footshock. Splenic NK cytotoxicity was determined by standard 4-h (51)Cr release assay. Percentages of lymphocytes were determined by flow cytometry. Plasma levels of ACTH, corticosterone, and prolactin concentration were measured by radioimmunoassay. After footshock, percentage of lysis relative to home-cage controls was 40% and 80% for sedentary and treadmill-trained animals, respectively (P < 0.05). Our results indicate that the protective effect of chronic exercise on innate cellular immunity in the Fischer 344 male rat is not restricted to activity wheel running, nor is it explained by elevations in basal NK activity, increased percentages of splenic NK and cytotoxic T cells, or increased plasma levels of ACTH, corticosterone, and prolactin.

Adrenocorticotropic Hormone↗

PubMed1998

Activity wheel running blunts increased plasma adrenocorticotrophin (ACTH) after footshock and cage-switch stress.

We examined whether chronic circadian physical activity attenuates hypothalamic-pituitary-adrenal hormone responses after footshock with or without cage-switch stress. Young (45 g) male Fischer 344 rats were randomly assigned to individual suspended home cages (HC) or cages with activity wheels (AW) (12 h:12 h light-dark photoperiod). After 6 weeks, each animal from a pair matched on mass (HC and AW) and average weekly running distance (AW) was randomly assigned to controllable or uncontrollable footshock on 2 days separated by 24 h. Half the animals were returned to the HC after the first day of shock, and half were switched to a new shoebox cage. One animal of each pair could end the shock for both rats by performing an FR-2 lever press. The yoked animal could not control the shock. After shock on Day 2, trunk blood was collected after decapitation. Plasma adrenocorticotrophin (ACTH), corticosterone, and prolactin were determined by radioimmunoassay. ANOVA for a 2 Group (AW vs. sedentary) x 2 Test (controllable vs. uncontrollable shock) x 2 Condition (HC vs. cage-switch) design indicated a Group x Test x Condition effect [F(1, 48) = 5.07, p = 0.03] and a Test main effect [F(1, 47) = 6.93, p = 0.01] for ACTH. ACTH was higher for sedentary animals after uncontrollable footshock under cage-switch conditions and higher after uncontrollable versus controllable footshock when averaged across groups and cage conditions. No effects were found for corticosterone or prolactin. Our results extend to activity wheel running prior findings of a cross-stressor attenuation in plasma [ACTH] in response to cage-switch after treadmill exercise training, though the cross-stressor effect was additive with footshock. Consistent with our prior reports, the cross-stressor effect of wheel running was not apparent after footshock administered under home-cage conditions.

Adrenocorticotropic Hormone↗

PubMed1997

Activity wheel running reduces escape latency and alters brain monoamine levels after footshock.

We examined the effects of chronic activity wheel running on brain monoamines and latency to escape foot shock after prior exposure to uncontrollable, inescapable foot shock. Individually housed young (approximately 50 day) female Sprague-Dawley rats were randomly assigned to standard cages (sedentary) or cages with activity wheels. After 9-12 weeks, animals were matched in pairs on body mass. Activity wheel animals were also matched on running distance. An animal from each matched pair was randomly assigned to controllable or uncontrollable inescapable foot shock followed the next day by a foot shock escape test in a shuttle box. Brain concentrations of norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 5-hydroxytryptamine (5-HT), and 5-hydroxyindole acetic acid (5-HIAA) were assayed in the locus coeruleus (LC), dorsal raphe (DR), central amygdala (AC), hippocampus (CA1), arcuate nucleus, paraventricular nucleus (PVN), and midbrain central gray. After prior exposure to uncontrollable foot shock, escape latency was reduced by 34% for wheel runners compared with sedentary controls. The shortened escape latency for wheel runners was associated with 61% higher NE concentrations in LC and 44% higher NE concentrations in DR compared with sedentary controls. Sedentary controls, compared with wheel runners, had 31% higher 5-HIAA concentrations in CA1 and 30% higher 5-HIAA concentrations in AC after uncontrollable foot shock and had 28% higher 5-HT and 33% higher 5-HIAA concentrations in AC averaged across both foot shock conditions. There were no group differences in monoamines in the central gray or in plasma prolactin or ACTH concentrations, despite 52% higher DA concentrations in the arcuate nucleus after uncontrollable foot shock and 50% higher DOPAC/DA and 17% higher 5-HIAA/5-HT concentrations in the PVN averaged across both foot shock conditions for sedentary compared with activity wheel animals. The present results extend understanding of the escape-deficit by indicating an attenuating role for circadian physical activity. The altered monoamine levels suggest brain regions for more direct probes of neural activity after wheel running and foot shock.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1996

Treadmill exercise training and estradiol increase plasma ACTH and prolactin after novel footshock.

We examined whether rats that were treadmill exercise trained (Tr) or chronically immobilized (CI) had similar responses by the hypothalamic-pituitary-adrenal (HPA) cortical axis to acute stress and whether the HPA responses interacted with the hypothalamic-pituitary-gonadal (HPG) axis. After 6 wk (1 h/day, 6 days/wk) of Tr or CI, plasma concentrations of adrenocorticotropic hormone ([ACTH]), [prolactin], and [corticosterone] were measured after familiar (treadmill running or immobilization) or novel (footshock) stress. Ovariectomized Sprague-Dawley females (n = 72) were implanted with capsules containing estradiol benzoate (E2) and randomly assigned in a 2-group (E2 vs. no E2) x 3 treatment (Tr vs. CI vs. sedentary) x 4 acute stressor [footshock vs. treadmill running (Run) vs. immobilization (Im) vs. no stress] x 3 recovery time (1 vs. 15 vs. 30 min) mixed-model analysis of variance. E2 capsules were removed from one-half of the animals 48 h before the first stressor session. After 10 min of acute stress, blood was drawn from a jugular catheter at 1, 15, and 30 min of recovery. [ACTH] and [prolactin] after footshock were higher in Tr rats with E2 compared with CI and sedentary rats without E2; recovery levels for sedentary animals were higher after Run compared with Im. The elevation in [corticosterone] from minute 1 to 15 of recovery was higher after the familiar Run and Im conditions. Our findings are consistent with an increased responsiveness of the HPA axis to novel footshock after treadmill exercise training that is additionally modulated by the HPG axis.

Adrenocorticotropic Hormone↗

PubMed1995

Stressors, including social conflict, decrease plasma prolactin in male golden hamsters.

Following exposure to a stressor, plasma prolactin (PRL) rises in most species. The purpose of the present study was to examine the effect of social conflict or of footshock stress on PRL responsiveness in male Syrian hamsters. Contrary to expectations, PRL was significantly lower in subordinate hamsters than in their dominant opponents or in controls following one, five, or nine exposures to social conflict. Similarly, PRL was reduced in hamsters subjected to a mild footshock stressor. By contrast, adrenocorticotropin, another stress-responsive hormone, was elevated following exposure to each of these stressors. We also demonstrate that PRL release is inhibited by dopamine as it is in other species by showing that there is a dose-dependent increase in PRL release following treatment with the dopamine receptor blocker, domperidone.

Adrenocorticotropic Hormone↗

PubMed1995

Treadmill exercise training and estradiol differentially modulate hypothalamic-pituitary-adrenal cortical responses to acute running and immobilization.

It is generally believed that physical fitness promotes health by attenuating responsiveness to other stressors. The experimental evidence for this belief is limited and does not extend to interactions between the hypothalamic-pituitary-adrenal cortical (HPA) and hypothalamic-pituitary-gonadal (HPG) axes. We tested the hypothesis that treadmill exercise training would lead to an estrogen-dependent hyporesponsiveness of the HPA axis that would generalize to immobilization stress. Ovariectomized female Sprague-Dawley rats (N = 74) that had been treadmill trained (TT) or sedentary for 6 weeks received intramuscular injections of estradiol benzoate (Eb) or sesame oil on each of 3 days prior to 15 min of acute treadmill running or immobilization. Plasma (adrenocorticotrophin) (ACTH), (corticosterone) (B) and (prolactin) (PRL) were determined from trunk blood by radioimmunoassay and compared in a 2 group (TT vs. sedentary)-by-2 treatment (Eb vs. oil)-by-2 acute stressor (running vs. immobilization) design. Home-cage (HC) animals (N = 24) provided baseline hormone levels. ACTH and B levels were elevated after stressors in animals treated with either Eb or oil compared to HC, but increases in PRL after stressors were dependent on Eb. Treadmill exercise training led to an attenuation of ACTH and prolactin to running, but the attenuation did not generalize to immobilization. In contrast, treadmill exercise training led to a hyperresponsiveness of ACTH. Treadmill training did not modulate prolactin responses to immobilization. The modulating effects of the estradiol treatment are consistent with an interaction of the HPA and HPG axes in response to stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1995

Activity-wheel running attenuates suppression of natural killer cell activity after footshock.

We studied whether voluntary running in an activity wheel moderates splenic natural killer (NK) cell cytotoxicity after footshock. Young (50-day) male Fischer 344 rats were randomly assigned to 1) sedentary (n = 16) or 2) activity-wheel (n = 16) groups that each received controllable or uncontrollable footshock on 2 consecutive days or 3) a sedentary home-cage control group (n = 8). Spleens and trunk blood were collected 30 min after the second footshock session. Cytotoxicity was determined by a standard 4-h 51Cr release assay. Percentages of OX6+ (B), OX8+ [T suppressor/cytotoxic (Ts/c)], W3/25+ (T helper), Thy-1.1 (Pan T cell marker), and 5C6+ (NK) cells were determined by flow cytometry. Plasma adrenocorticotropic hormone, corticosterone, and prolactin concentrations were measured by radioimmunoassay as modulators of NK activity. Percentage of specific lysis after footshock was approximately 52% of control values for sedentary animals compared with approximately 96% of control values for activity-wheel animals. The groups did not differ in percentages of NK or Ts/c cells. We conclude that voluntary activity-wheel running protects against the suppression of splenic NK activity induced by footshock. This protective effect of wheel running is not explained by an elevation in baseline NK activity; increased percentages of splenic NK or Ts/c cells; or plasma levels of adrenocorticotropic hormone, corticosterone, and prolactin.

Adrenocorticotropic Hormone↗

PubMed1995

Whole-body irradiation transiently diminishes the adrenocorticotropin response to recombinant human interleukin-1 alpha.

Recombinant human interleukin-1 alpha (rhIL-1 alpha) has significant potential as a radioprotector and/or treatment for radiation-induced hematopoietic injury. Both IL-1 and whole-body ionizing irradiation acutely stimulate the hypothalamic-pituitary-adrenal axis. We therefore assessed the interaction of whole-body irradiation and rhIL-1 alpha in altering the functioning of the axis in mice. Specifically, we determined the adrenocorticotropin (ACTH) and corticosterone responses to rhIL-1 alpha administered just before and hours to days after whole-body or sham irradiation. Our results indicate that whole-body irradiation does not potentiate the rhIL-1 alpha-induced increase in ACTH levels at the doses used. In fact, the rhIL-1 alpha-induced increase in plasma ACTH is transiently impaired when the cytokine is administered 5 h after, but not 1 h before, exposure to whole-body irradiation. The ACTH response may be inhibited by elevated corticosterone levels after whole-body irradiation, or by other radiation-induced effects on the pituitary gland and hypothalamus.

Adrenalectomy↗

PubMed1994

Decreased vasopressin content in parvocellular CRH neurosecretory system of Lewis rats.

Rats possess stress-responsive, vasopressin (VP)-expressing and stress-nonresponsive, VP-deficient subpopulations of parvocellular corticotropin-releasing hormone (CRH) neurosecretory cells. Both subpopulations are activated by bacterial lipopolysaccharide (LPS) and cytokines. Lewis rats exhibit hyporesponsive hypothalamo-pituitary-adrenocortical axes (HPAAs). The Lewis CRH neurosecretory system has been reported to be defective in females and normal in males. We used post-embedding electron microscopic (EM) immunocytochemistry to study baseline levels and LPS-stimulated depletion of neurosecretory vesicles. Male Lewis rats possessed normal numbers of CRH+/VP- varicosities and low numbers of CRH+/VP+ varicosities, indicating abnormally low release of VP into portal blood. This defect contrasts with the reported increase in VP content and release in magnocellular neurosecretory cells in Lewis rats.

Animals↗

PubMed1994

Systemically administered histamine H1 and H2 receptor antagonists do not block the ACTH response to bacterial lipopolysaccharide and interleukin-1.

The administration of lipopolysaccharide (LPS) results in the activation of the hypothalamic-pituitary-adrenal axis (HPAA). We recently reported that the participation and interaction of LPS-induced proinflammatory cytokines were obligatory for the stimulation of adrenocorticotropic hormone (ACTH) release by LPS. LPS and LPS-derived cytokines also stimulate the release of histamine (HA). HA is a known hypothalamic neurotransmitter and activates the HPAA. Therefore, to elucidate the role of HA in LPS- and cytokine-induced ACTH release, we evaluated the effects of several HA H1 and H2 receptor antagonists on the ACTH response to LPS, recombinant human interleukin-1 alpha (rhIL-1 alpha) and HA in mice. Although all 3 of the H1 receptor antagonists administered (mepyramine (MEP), diphenhydramine (DPH) or promethazine (PMZ) were able to block the 10-min ACTH response to HA, only PMZ (a less selective H1 receptor antagonist than MEP) was able to reduce the LPS- or rhIL-1 alpha-induced ACTH responses. Ranitidine, a powerful and selective H2 receptor antagonist, had little effect on the LPS- and rhIL-1 alpha-induced ACTH responses, while metiamide (MET), a much less potent first-generation H2 receptor antagonist, substantially diminished ACTH release. The greater effectiveness of PMZ, in contrast to MEP or DPH, probably relates to the ability of phenothiazine derivatives to inhibit non-HA-dependent pathways involved in the stimulation of the HPAA by cytokines; the same may be true of MET.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1993

Synergistic roles of interleukin-6, interleukin-1, and tumor necrosis factor in the adrenocorticotropin response to bacterial lipopolysaccharide in vivo.

Administration of lipopolysaccharide (LPS) results in activation of the hypothalamic-pituitary-adrenal axis. LPS induces the release of a number of proinflammatory cytokines, i.e. interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF), which activate the hypothalamic-pituitary-adrenal axis as well and may mediate the effects of LPS. Variations in the kinetics of appearance of IL-1, TNF, and IL-6 after LPS challenge suggested that these cytokines may play different roles at different times. To elucidate the mutual dependence and contribution of individual cytokines in the course of LPS-induced ACTH release, we used blocking antibodies to IL-6, TNF, and the IL-1 receptor. Our results demonstrate that anti-IL-6 antibody abrogated ACTH induction throughout the course of the response both 2 and 4 h after LPS challenge. In contrast, anti-IL-1 receptor and anti-TNF antibody, given individually, blocked ACTH production at 4 h, but not at 2 h. Only combined administration of these two antibodies diminished, but did not eliminate, ACTH release at 2 h. This is the first demonstration that all three inflammatory cytokines are obligatory for LPS-induced elevation of plasma ACTH. In addition, these results suggest that IL-1, IL-6, and TNF play different roles in LPS-induced ACTH release.

Adrenocorticotropic Hormone↗

PubMed1992

Hormonal responses to fighting in hamsters: separation of physical and psychological causes.

Male Syrian hamsters were paired and allowed to interact with a conspecific for 15 min a day for 4 days. On the fifth day, the animals were again paired, but they were kept physically separated by a mesh partition that allowed visual, olfactory, and auditory contact between the animals. Controls were placed with conspecifics on each of the 5 testing days, but the partition between them was never removed. Hamsters that were submissive on days 1-4 exhibited elevated plasma adrenocorticotropin-like immunoreactivity (ACTH-LI), beta-endorphin-like immunoreactivity (B-EP-LI), and cortisol on day 5 even though no fighting occurred on that day. Dominant hamsters did not differ from controls. These data support the hypothesis that there is an important psychological component to the pituitary-adrenocortical response in defeated hamsters.

Adrenocorticotropic Hormone↗

PubMed1992

Effects of controllable vs. uncontrollable chronic stress on stress-responsive plasma hormones.

We have previously reported effects of chronic stress on circadian rhythms of temperature, eating, and locomotor activity. These studies were conducted using an around-the-clock signalled intermittent footshock paradigm in which some rats have control over shock termination while other rats are yoked to the rats with control. Although this paradigm is stressful, as suggested by decreases in food intake and disrupted circadian rhythms, rats tolerate the paradigm well, continuing to eat, drink, gain weight, and groom. In the present studies, rats were sacrificed following 3 or 14 days of stress, and plasma was collected for hormonal assays. After 3 days of stress, plasma corticosterone and prolactin levels were elevated in both stress groups compared to controls; yoked rats had higher levels of corticosterone than rats in the group with control over shock termination, while prolactin levels in both stressed groups were similar. ACTH levels were similar in stressed and control rats. After 14 days of stress, ACTH and corticosterone levels in both stress groups were similar to control levels. Prolactin levels were elevated in the yoked experimental group compared to levels in control or controllable stress groups. These data support previous studies suggesting that control over stressors attenuates the effects of stress on physiology and demonstrate that two hormones with diverse biological effects are elevated by chronic stress.

Adrenocorticotropic Hormone↗

PubMed1992

Effects of interleukin-1 on the stress-responsive and -nonresponsive subtypes of corticotropin-releasing hormone neurosecretory axons.

Administration of interleukin-1 (IL-1) induces increases in plasma ACTH and glucocorticoids. Numerous experiments have implicated the hypothalamic CRH neurosecretory system in these responses, but have failed to provide evidence for involvement of the ACTH secretagogue vasopressin (VP). The rat CRH neurosecretory system contains two types of cells: VP expressing and VP deficient. Hence, the above findings suggested that IL-1 may selectively activate the VP-deficient subtype of CRH neurosecretory cells. In this study we employed postembedding electron microscopic immunocytochemistry to directly assay IL-1-induced depletion of secretory vesicles from identified VP-expressing and VP-deficient CRH neurosecretory axons. IL-1-induced depletion of secretory vesicles from these axons was correlated with increases in plasma ACTH and decreases in plasma PRL. No dose of IL-1 was found that could selectively activate one subtype of CRH neurosecretory axons; at doses of 0.67 microgram/100 g and above for both IL-1 alpha and IL-1 beta, equal depletion of vesicles from the two subtypes was observed. Similar results were previously found after the injection of bacterial lipopolysaccharide, which induces the release of IL-1 from macrophages. The findings unequivocally establish for the first time that IL-1 activates hypothalamic CRH neurosecretory cells in the absence of surgical stress, anesthesia, disruption of the infundibular area, or administration of toxic drugs. In addition, these data clearly demonstrate that IL-1 induces the release of VP from neurosecretory axons in the portal capillary zone of the external zone of the median eminence. Previous studies have shown that the VP-deficient subtype of CRH neurosecretory axons is not strongly activated by several types of stress; therefore, activation of the system by inflammatory mediators involves mechanisms different from those mediating the stress response.

Adrenocorticotropic Hormone↗

PubMed1991

Acute and repeated exposure to social conflict in male golden hamsters: increases in plasma POMC-peptides and cortisol and decreases in plasma testosterone.

The purpose of the present study was to characterize the hormonal response of dominant and submissive male hamsters to acute and repeated exposure to social conflict. We found that submissive, but not dominant, males exhibited elevated plasma levels of adrenocorticotropin (ACTH), cortisol, and beta-endorphin (beta-EP) following one exposure to an agonistic encounter. After five exposures to a dominant opponent, submissive males showed smaller, but still significant, elevations in these plasma hormones. After nine exposures, submissive hamsters showed significant elevations only in plasma ACTH and beta-EP. Plasma testosterone was significantly suppressed in submissive males that fought nine times. We conclude that hamsters are a useful species with which to study the neuroendocrine correlates of social behavior.

Adrenocorticotropic Hormone↗

PubMed1991

Interleukin-1 and interleukin-6 act synergistically to stimulate the release of adrenocorticotropic hormone in vivo.

Interleukin-1 (IL-1) and interleukin-6 (IL-6) share a number of biological functions. Because IL-1 induces IL-6 in vivo, the extent to which IL-6 mediates the effects of IL-1 has come under investigation. The stimulation of the hypothalamic-pituitary-adrenal axis by IL-1 and IL-6 is a critical component of the inflammatory response. The present study was designed to compare the effects of recombinant human IL-1 alpha (rhIL-1 alpha) and recombinant human IL-6 (rhIL-6) administered in combination and alone on the release of adrenocorticotropic hormone (ACTH) in mice. We have demonstrated that the administration of rhIL-6 alone does not duplicate the stimulatory effect of rhIL-1 alpha on ACTH release. On the other hand, suboptimal amounts of rhIL-1 alpha and rhIL-6 synergize to induce an early (30-60 min) ACTH response and produce a later (2-3 h) response that is similar to the one observed after rhIL-1 alpha is administered alone. These results suggest that the 2-3 h response to rhIL-1 alpha may be dependent on synergy with the endogenous IL-6 it induces systemically and in the central nervous system (including the hypothalamus and the pituitary gland).

Adrenocorticotropic Hormone↗

PubMed1990

Neuroendocrine responses to emotional stress: possible interactions between circulating factors and anterior pituitary hormone release.

We have shown that a psychological stressor can elicit increases in plasma AVP levels in normal human subjects. Since AVP can enhance the release of ACTH, and the pituitary gland is outside the blood-brain barrier, AVP present in the general circulation might extend the time course of stress-induced, CRF-mediated release of ACTH from the anterior lobe. Since PRA is involved in the synthesis of angiotensin I, the precursor of AII, and AII is known to enhance CRF-mediated release of ACTH from pituitary cells and to stimulate release of AVP, it is possible that the increase in PRA also contributed to the release of AVP and ACTH in this study. Reports differ as to whether circulating catecholamines can release ACTH in vivo by direct action on the pituitary. Finally, it has been reported that beta-EP enhances the release of PRL, and inhibits release of AVP. Since the increase in beta-EP in the present study was quite robust, it might have extended the PRL release, and truncated the AVP response.

Adrenocorticotropic Hormone↗