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PubMed1993

Biphasic effect of ACTH on growth of rat adrenocortical cells in primary culture.

The proliferation rate of differentiating fetal rat adrenocortical cells was studied in primary culture. In this system, stimulation with ACTH induces differentiation of zona glomerulosa-like cortical cells into zona fasciculata-like cells. Incorporation of bromodeoxyuridine (BrdU) was studied immunocytochemically by use of anti-BrdU antibody, and the proliferation rate was counted from the monolayer colonies of adrenocortical cells. After 21 days of cultivation in the absence of ACTH, the proliferation rate of zona glomerulosa-like cells was 10%. The rate slowly declined to 1% at the age of 100 days during continuous cultivation in the absence of ACTH. Stimulation with ACTH induced a strong inhibition in the proliferation rate (down to 2% during the first 24 h). Treatment with ACTH during the following 48 h led to an extremely intense proliferation of adrenocortical cells at a proliferation rate of 25%. Continuous treatment with ACTH up to 100 days led to a persistent growth of adrenocortical cells, and a proliferation rate over 2-fold higher than in control cells cultivated in the absence of ACTH. Thus, ACTH is the principal growth-promoting factor also in vitro, as has been found in in vivo studies. This growth effect is mediated by a biphasic course; at the beginning of differentiation the effect is inhibitory and is followed by a persistent stimulation of the growth of adrenocortical cells.

Adrenal Cortex↗
PubMed1989

Immunocytochemical localization of ACTH-like immunoreactivity in rat adrenal glomerulosa and fasciculata cells.

The role of ACTH in the synthesis of the adrenocortical hormones has been largely described. In order to investigate the localization of this peptide at the subcellular level of the adrenal glomerulosa and fasciculata cells, an immunocytological method was used. Rat adrenals were fixed and frozen. Ultrathin sections obtained by cryoultramicrotomy, were incubated with anti-beta (1-24) ACTH or anti-alpha (17-39) ACTH sera. The antigen-antibody reaction was detected by PAP complexes (revealed by 4-chloro-1-naphthol) or with protein A-colloidal gold or IgG-colloidal gold. The results obtained were the same whatever the antisera of the technique employed. All the cells of the adrenal zona glomerulosa and zona fasciculata were labelled. ACTH-like immunoreactivity in zona glomerulosa and zona fasciculata cells was observed at the plasma membrane level, in cytoplasmic matrix, mitochondria and nucleus (in the euchromatin close to the heterochromatin aggregations and, occasionally, associated with the nucleolus). No immunoreactivity was observed when non-immune serum or anti-ACTH serum preincubated with ACTH were used, nor there was any modification of the immunocytochemical reaction when anti-ACTH serum incubated with heterologous antigens was employed. These data, demonstrate the presence of endogenous ACTH in both adrenal glomerulosa and fasciculata cells, and suggest that the peptide is internalized after binding to the plasma membrane.

Adrenocorticotropic Hormone↗
PubMed1983

Circadian and seasonal changes in ACTH-induced effects in healthy young men.

The effects of the ACTH 1-17 analogue (100 micrograms i.m.) as a function both of time of day (7.00, 14.00 and 21.00 h) and season (winter versus summer) were determined on a set of physiological variables: urinary 17-hydroxycorticosteroids, oral temperature, grip strength (right and left hands), peak expiratory flow and self - rated fatigue. Six young healthy males took part in the study in January-February 1980 and June-July 1981. They were synchronized with a diurnal activity from 7.00 to midnight and a nocturnal rest. Urine was collected every 3 to 4 hours, at fixed clock hours over 72 h (winter) and 48 h (summer). There was a one week interval between each ACTH test or placebo control. Variables were measured according to the same schedule. 24 h urinary 17-OHCS excretion was maximum for ACTH injected at 7.00 in winter and 14.00 in summer, and the minimum occurred after ACTH given at 21.00. The highest peak of urinary 17-OHCS was found after ACTH at 7.00 both in winter and in summer. It is likely that the maximal stimulation of glucocorticoid secretion occurs when ACTH is administered around the beginning of the activity span. Both in winter and summer the injection of ACTH at 7.00 was followed by the greatest decrease in self-rated fatigue (24 h mean) and the largest increase (24 h mean) both in grip strength and peak expiratory flow (bronchial patency) in comparison with other times of ACTH administration (14.00 and 21.00 h).

17-Hydroxycorticosteroids↗
PubMedDate not supplied

Modulation of adrenal cell functions by cadmium salts. 1. Cadmium chloride effects on basal and ACTH-stimulated steroidogenesis.

Cultured Y-1 mouse adrenal tumor cells, which secrete 20-alpha-hydroxy-4-pregnen-3-one (20-DHP), were used to investigate the acute nonlethal effects of incremental cadmium chloride (CdCl2) concentrations on basal and maximally stimulated steroid secretion. In addition, cumulative CdCl2 effects during 4-hr incubations, effect reversibility, and viability were determined. Cells were incubated in 1 ml serum-free Eagle's Minimal Essential Medium (FMEM) with or without 0.5 IU (ca. 1.5 microM) adrenocorticotropin (ACTH) in the presence or absence of CdCl2. Following incubation, cell viability was quantitated using trypan blue exclusion. The 20-DHP secreted into the experimental incubation medium was measured by radioimmunoassay. CdCl2 levels of 10.0 micrograms/ml or greater significantly inhibited basal 30 min steroid secretion in a dose-dependent manner; ACTH-stimulated steroid secretion was significantly inhibited by levels 5.0 micrograms/ml or greater. At least 80% of all control and stimulated cells in the presence or absence of cadmium ions excluded trypan blue. The reduction in ACTH-stimulated steroid secretion was greater than the reduction in basal steroid secretion at any cadmium concentration level. The CdCl2 concentration that reduced stimulated steroid hormone secretion by 50% (IC50) was 45.0 micrograms/ml. Exposing Y-1 cells to either 5.0, 10.0, 45.0 or 500.0 micrograms CdCl2/ml FMEM for periods ranging from 0.5 to 4 hr inhibited ACTH-stimulated steroid secretion in a time-dependent manner. After 30 min exposure to 10.0, 45.0 or 500.0 micrograms CdCl2/ml FMEM with or without ACTH, cadmium inhibition was irreversible. When 5.0 micrograms CdCl2/ml was used, basal and stimulated inhibition was reversible by reincubating in medium containing ACTH alone. The relatively greater cadmium effects on ACTH stimulated steroidogenesis might suggest that cadmium modulated the rate-limited transducing system between the ACTH plasma membrane receptor complex and cholesterol side-chain cleaving mitochondrial enzymes. However, cadmium influences on basal secretion indicated effects on the non-rate-limited steroidogenic pathway.

20-alpha-Dihydroprogesterone↗
PubMed1984

Evidence for ACTH-unrelated mechanisms in the regulation of cortisol secretion in man.

In an attempt to elucidate the significance of ACTH independent mechanisms in the regulation of cortisol secretion in man, the dynamics of plasma ACTH and cortisol levels were studied in response to different stimuli. The cortisol response to small amounts of exogenous ACTH and to insulin induced hypoglycemia was preceded by an increase in ACTH levels appropriate to explain the increase in cortisol. In contrast, after administration of methamphetamine, there was an increase in cortisol levels in the absence of any changes in ACTH concentrations. Apparently, the methamphetamine induced cortisol secretion was not mediated by radioimmunoassayable ACTH. A diurnal rhythm was observed for the responses to hypoglycemia and to methamphetamine with larger cortisol responses in the evening as compared to the forenoon. These changes were not accompanied by parallel changes in the ACTH responses. From these differences, additional evidence is provided for the importance of ACTH independent mechanisms in the regulation of cortisol secretion.

Adrenal Cortex↗
PubMed1981

Response of white adipocyte of mouse and rabbit to catecholamines and ACTH. 2. Stability and restoration of activity of hormone-sensitive adenylate cyclase of adipocyte plasma membrane.

The isolated intact white adipocyte of the Swiss mouse responds to both ACTH and catecholamines by an elevation of cAMP levels and an increase in lipolysis. However, in the isolated plasma membrane of the mouse adipocyte, adenylate cyclase loses its responsiveness to ACTH but retains its ability to respond to catecholamines. This lack of responsiveness to ACTH by adenylate cyclase of mouse adipocyte plasma membrane can be overcome, at least partially, by addition of GPP (NH)p, an analog of GTP, to the assay medium. The data on mouse adipocyte membrane suggests that the coupling of ACTH receptor to adenylate cyclase is dependent on GTP and that catecholamine-activation of adenylate cyclase is less dependent on this nucleotide. The isolated intact white adipocyte of adult New Zealand rabbit responds to ACTH, but does not (or only weakly) respond to catecholamines. In contrast to the mouse plasma membrane preparation, adenylate cyclase of adipocyte membrane of the rabbit responds to ACTH. And the addition of GPP(NH)P is not required to demonstrate the CTH: sensitive adenylate cyclase activity. The difference between mouse and rabbit adipocyte membrane in the requirement for GPP(NH)P in ACTH action is not readily explained. The lack of catecholamine sensitivity of rabbit membrane enzyme cannot be reversed by addition of GPP(NH)P or adenosine deaminase. These two adenylate cyclase model systems using mouse and rabbit adipocyte plasma membrane may be useful tools for the study of the specificity and mechanism of action of lipolytic hormones such as ACTH and catecholamines.

Adenylyl Cyclases↗
PubMed1983

Effect of solution of low pH on releases of beta-endorphin-like immunoreactivity and ACTH-like immunoreactivity from human gastric antral mucosa in vitro.

The presence of beta-endorphin-like and ACTH-like immunoreactivities (beta-EpLI, and ACTH-LI, respectively) in human gastric antral mucosa and their release were studied. beta-EpLI (14.1 +/- 4.8 ng/g wet weight) and ACTH-LI (11.1 +/- 1.2 ng/g wet weight) were detected in human gastric antral mucosa. The two activities gave similar curves for inhibition of human beta-Ep and ACTH on radioimmunoassay, respectively. On gel-filtration chromatography of a gastric antral extract, three components of beta-EpLI and two components of ACTH-LI were separated. When human gastric antral mucosa was incubated with a solution of pH 4.0 or pH 2.0, the release of beta-EpLI and ACTH-LI from the mucosa into the incubation medium increased 2.3-9.8-fold. However, incubation with 20 mM glucose or 20 mM amino acids did not have any effect on the release of beta-EpLI and ACTH-LI. These results indicate that beta-EpLI and ACTH-LI present in human gastric antral mucosa are released by direct action of a solution of low pH on the gastric antral mucosa.

Adrenocorticotropic Hormone↗
PubMed1986

Cinemicrographic observations of cultured adrenocortical tumor cells. Dynamic responses to ACTH and cytochalasin B.

ACTH increases the basal steroidogenic activity of cultured adrenocortical tumor cells, whereas moderate-high doses of cytochalasin B (CB) inhibit both basal and ACTH-induced steroidogenesis. Previous ultrastructural studies have revealed that ACTH rearranges microfilaments in these adrenal cells, whereas CB causes microfilaments to aggregate into felt-like masses. It has been postulated that the ACTH effects may facilitate organelle motility and increase organelle interactions that are required for steroid biosynthesis, and that the CB-created "foci" may impede or prevent the organelle meetings. To shed light on these possibilities, we have employed 16 mm cinemicrography of unstimulated adrenal tumor cells and cells incubated for 1-2 h with ACTH (10 mU/ml), or low (10 micrograms/ml), or high (50 micrograms/ml) doses of CB. ACTH caused initial increases in membrane ruffling and a "flurry" of particle (organelle) activity above that seen in unstimulated cells. The stimulated cells then retracted from each other and began their characteristic "rounding up" in response to the hormone. Particles appeared to move towards the nucleus, and in fully-rounded cells were extremely congested. Steroid production rose several fold above basal levels. CB10 produced slight-marked cell convexities, nearly stopped particle motility and inhibited steroid production moderately. CB50 produced an asymmetrical, spidery cell form, stopped membrane ruffling and particle motility and abolished steroidogenesis. After a washout of CB50, particle motility resumed nearly immediately. Our CB data indicate that associations between particles, presumably between mitochondria and various sources of cholesterol, are prerequisite for basal steroidogenesis in the adrenal tumor cells. In ACTH-stimulated cells, increases in steroid output correspond with increased opportunities for particle associations. These opportunities appear to arise directly or indirectly from ACTH effects on microfilaments. The responses of microfilaments to the hormone may be particularly intense in tumorous forms. By these means, the cells may express their differentiated function, although their cytoplasm has a distinctly unspecialized appearance.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

ACTH 1-17 effects on intermediary metabolites in healthy subjects.

Some acute and chronic metabolic effects of a new ACTH analogue (ACTH 1-17, Synchrodyn) were evaluated in healthy subjects and compared to those of the synthetic fragment ACTH 1-24. The peptides were injected at doses reportedly comparable with regard to their corticotropic effect, i.e. 100 micrograms ACTH 1-17 and 250 micrograms ACTH 1-24. A similar increase in blood glucose, NEFA and ketone bodies concentrations, without any significant modification of insulin, C-peptide and glucagon levels, was observed after injecting both peptides. The chronic treatment with ACTH 1-24 induced a significant increase in basal lactate, pyruvate and alanine blood concentrations. The levels of these metabolites resulted unaffected or slightly reduced after the corresponding treatment with ACTH 1-17. Our data are compatible with a certain degree of exhaustion of the adrenocortical reserve or, alternatively, a resetting of the circadian cortisol rhythm after prolonged treatment with the ACTH 1-17 analogue.

Adrenocorticotropic Hormone↗
PubMed2000

Repetitive graded ACTH stimulation test for adrenal insufficiency.

ACTH stimulation is useful in assessing the hypothalamo-pituitary-adrenal axis. However, there is still some debate about the proper dose and interpretation. We designed a new protocol using repetitive graded ACTH stimulation. Thirty-two patients with the diagnosis of adrenal insufficiency (Al) were studied. After taking samples for baseline ACTH and cortisol, 1 microg fresh-prepared ACTH (Synacthen (1-24)) was injected intravenously, then 5, 50 and 100 microg at hourly interval. Cortisol responses were measured at 30, 60, 120, 180 and 240 min. The secondary Al group (26 subjects) had cortisol responses in between those of the control group (8 subjects) and the primary Al group (6 subjects). The minimal overlap between the secondary Al group and the control group occurred at a 30-min cortisol response after 1 microg ACTH stimulation, using 20 microg/dl as the cut-off level. There was only one exception which showed an episodic release at 30 min. There were 5, 10 and 9 patients with secondary Al who responded normally to 5, 50 and 100 microg ACTH stimulation, respectively. Maximal cortisol increments of the primary Al group were all below 4 microg/dl. Although there were 11 cases of secondary Al whose cortisol responses overlapped with those of primary Al, only two of them had a cortisol increment less than 4 microg/dl. Our new protocol combines the advantage of the low dose ACTH stimulation test, a sensitive method for detecting mild Al, and the ACTH infusion test, a longer test to mimic surgical stress.

Adrenal Insufficiency↗
PubMed2000

Comparative analysis of plasma 17-hydroxyprogesterone and cortisol responses to ACTH in patients with various adrenal tumors before and after unilateral adrenalectomy.

Patients with non-hyperfunctioning adrenal adenomas often have an increased plasma 17-hydroxyprogesterone response to ACTH stimulation. The effects of adrenal surgery on this abnormality have rarely been investigated. One hundred and sixty-one patients with unilateral adrenal tumors (non-hyperfunctioning adenomas, 78; cortisol-producing adenomas, 8; aldosterone-producing adenomas, 37; adrenal cysts, 12; pheochromocytomas, 26) were studied. Patients before and after adrenal surgery as well as 60 healthy subjects underwent an ACTH stimulation test using 2 mg synthetic ACTH(1-24) (Cortrosyn Depot, Organon). Basal and ACTH-stimulated plasma 17-hydroxyprogesterone and cortisol concentrations are reported. Before adrenal surgery, the basal plasma 17-hydroxyprogesterone concentrations were normal in patients with all types of tumors. However, the ACTH-stimulated plasma 17-hydroxyprogesterone levels were abnormally increased in 53% and 31% of patients with non-hyperfunctioning adenomas and aldosterone-producing adenomas, respectively. In addition, a few patients with adrenal cysts and pheochromocytomas also showed an increased ACTH-stimulated 17-hydroxyprogesterone response. After unilateral adrenalectomy, this hormonal abnormality disappeared in most, although not all patients with adrenal tumors. In patients with non-hyperfunctioning adrenal tumors, ACTH-stimulated plasma 17-hydroxyprogesterone and cortisol concentrations significantly correlated with the size of the tumors. These results firmly indicate that the tumoral mass itself may be responsible for the increased plasma 17-hydroxyprogesterone and cortisol responses after ACTH stimulation in patients with non-hyperfunctioning and hyperfunctioning adrenal adenomas.

17-alpha-Hydroxyprogesterone↗
PubMed1996

Localization of ACTH receptor mRNA by in situ hybridization in mouse adrenal gland.

Stimulation of steroidogenesis in the adrenal cortex is a major physiological action of adrenocorticotropic hormone (ACTH). This action is presumed to be mediated by the ACTH receptor and is functionally connected with the hypothalamus-pituitary-adrenal axis. To gain information concerning the distribution of the ACTH receptor in this axis, we examined mRNA for the ACTH receptor in the adrenal gland, pituitary and hypothalamus of the mouse, by using in situ hybridization. The Y-1 mouse adrenal tumour cell line was also examined. The specific hybridization signal for ACTH receptor mRNA was uniformly distributed in the Y-1 cells, although the level of expression was low. The adrenal cortex showed a strong signal for the ACTH receptor mRNA in both the zona fasciculata and the zona glomerulosa, sites that are involved in the mediation of the action of ACTH on the synthesis and release of glucocorticoids and aldosterone. In the zona reticularis of the cortex, a small number of cells showed positive hybridization signals. Moreover, a few scattered cells were positive in the adrenal medulla. In contrast, the hybridization results for both the hypothalamus and the pituitary proved to be negative. These results indicate that the mouse ACTH receptor is a peripheral receptor that is exclusively located in the adrenal gland.

Adrenal Glands↗
PubMed1990

Nocturnal and early morning secretion of ACTH and cortisol in humans.

It is well established that the adrenocorticotropic hormone (ACTH) stimulates the synthesis and release of cortisol from the adrenal cortex, but the role of ACTH in the physiological regulation of basal cortisol secretion has received surprisingly little study. The authors studied the nocturnal and early morning secretory pulses of cortisol and ACTH in normal subjects. A pulse detection algorithm was developed. The relationship between ACTH and cortisol pulses in terms of temporal and proportional relationship is described. Pulse concomitance for ACTH with cortisol was 47% and for cortisol with ACTH pulses it was 60%. The first description of the relationship between concomitant ACTH and cortisol pulse magnitudes in humans is presented. A highly significant linear relationship between the magnitudes of ACTH and cortisol pulses is shown. Putative reasons for dissociated pulses and the potential implication of these findings are discussed.

Adrenocorticotropic Hormone↗
PubMed1994

Elevation of plasma ACTH concentration in rabbits made febrile by systemic injection of bacterial endotoxin.

This study was carried out to investigate the adrenocorticotropic hormone (ACTH) response in rabbits made febrile by systemic injection of lipopolysaccharide (LPS, Salmonella typhosa endotoxin). Intravenous (i.v.) injection of LPS (0.1 microgram/kg and 1.0 microgram/kg) increased rectal temperature (biphasic fever) and the plasma concentration of ACTH (ACTH response) in a dose-related manner. These responses were suppressed by pretreatment with indomethacin (20 mg/kg, subcutaneously). Intracerebroventricular (i.c.v.) administration of indomethacin (400 micrograms) had no effect on the ACTH response to LPS, although it significantly suppressed febrile response. Small increases in plasma concentration of ACTH and significant fevers followed i.c.v. administration of prostaglandin E2 (2 micrograms) or F2 alpha (2 micrograms). I.v. administration of corticotropin releasing factor (CRF) antagonist [alpha-helical CRF (9-41) (200 micrograms/kg)] partly suppressed the ACTH increase induced in plasma by i.v. LPS. These results suggest that prostaglandins synthesized outside the blood-brain barrier play an important role in the ACTH response and that the mechanism for induction of the ACTH response is not exactly the same as that for the febrile response, although prostaglandins are involved in both responses.

Adrenocorticotropic Hormone↗
PubMed1988

Post-translational processing of pro-opiomelanocortin (POMC)-derived peptides during fetal monkey pituitary development. I. Adrenocorticotropin (ACTH) and alpha-melanotropins (alpha-MSHs).

We have studied the post-translational processing of POMC-derived peptides during fetal monkey development using immunoassay and reverse-phase high-performance liquid chromatography (RP HPLC). Pituitary tissues obtained from fetal monkeys ranging from Gestational Day 50 to 155 were fractionated and analyzed for ACTH- and alpha-MSH-related peptides and compared to adult forms. Extracts of whole pituitary from Fetal Days 50 and 55 contained ACTH(1-39) and very small amounts of CLIP (corticotropin-like intermediate-lobe peptide; ACTH(18-39))-like immunoactivity. Acetylated alpha-MSHs were not detectable at Day 50. alpha-MSHs were barely detectable at Day 55. By Day 65, when pituitary lobes were separable, small amounts of des-, mono-, and diacetyl alpha-MSH were detectable in NIL extracts, but not in anterior lobe extracts. ACTH(1-39) levels were negligible when compared to increasing alpha-MSHs through Fetal Day 80 to 155 in the intermediate lobe. The CLIP immunoactivity was negligible in Day 80 and adult anterior lobe extracts. Thus, lobe-specific proteolytic processing of ACTH-related peptides was well established by midterm gestation. Marked increases of alpha-N- and alpha-N,O-acetylated forms of alpha-MSHs were detected during middle and late stage fetal development. Diacetyl alpha-MSH was the predominant form of alpha-MSH in adult NIL extracts. No acetylated alpha-MSHs were found in anterior lobe tissues, thus adult anterior lobe extracts contained almost exclusively ACTH(1-39). However adult NIL extracts contained two distinct forms of CLIP-related immunoactivity. Therefore changes in post-translational processing patterns of ACTH-related and alpha-MSH-related peptides continued to some extent, postnatally. These data indicate that marked changes in post-translational processing of POMC-derived ACTH-related products occur during the first half of monkey gestation.

Adrenocorticotropic Hormone↗
PubMed1980

Opiate receptors may mediate the suppressive but not the excitatory action of ACTH on motor activity in rats.

Subcutaneous injections of adrenocorticotropin (ACTH) or of the opiate antagonist naltrexone produced a one (2.0 mg/kg) dpressed, whereas smaller doses of ACTH (50 micrograms/kg) and of naltrexone (0.125 and 0.25 mg/kg) stimulated motor activity in the open field test. Furthermore, naltrexone at a dose level that had no effect on motor activity blocked the suppressive effect of the high doses of ACTH but had no effect on the stimulating effect of the intermediate dose of ACTH. Finally, chronic naltrexone administration resulted in enhanced sensitivity to the suppressive but not to the stimulating effect of ACTH on motor activity. It is argued that opiate receptors may play a selective role in the effect of ACTH on motor activity. Such receptors may mediate the supressive effect of high doses of ACTH whereas other, naltrexone insensitive receptor systems may mediate the stimulating effect of ACTH on activity functions.

Adrenocorticotropic Hormone↗
PubMed1987

Stimulation by angiotensins I and II of ACTH release from goldfish pituitary cell columns.

Dispersed, superfused goldfish anterior pituitary cell columns were stimulated with pulses of salmon angiotensin I (sAI), human angiotensin I (hAI), and human angiotensin II (hAII). Human AII stimulated the greatest release of ACTH. The dose-response curves for hAI and sAI were similar and revealed that hAI and sAI were about one-tenth as potent as hAII in stimulating ACTH release. In mammals, AI must be converted to AII in order to stimulate ACTH release. In goldfish, the angiotensin-converting enzyme inhibitor captopril, which inhibits the conversion of AI to AII, was not able to block sAI-stimulated ACTH release. This finding suggests that the angiotensin receptor of the goldfish corticotrope is less discriminating than that of the mammalian corticotrope and recognizes both AI and AII. This hypothesis was supported by the observation that sarcosine analogs of AII, which block AII-stimulated ACTH release in mammals, failed to block hAII-stimulated ACTH release in goldfish. Saralasin showed negligible, [Sar1,Thr8]-AII slight, and [Sar1, Ile8]-AII moderate, intrinsic ACTH-releasing activity. These findings suggest that the ACTH-releasing activity of angiotensin appeared early in the evolution of the vertebrate pituitary.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1992

Stress response in the freshwater snail Planorbarius corneus (L.) (Gastropoda, Pulmonata): interaction between CRF, ACTH, and biogenic amines.

Previous studies reported that ACTH molecules influence chemotactic and phagocytic activities of hemocytes in the freshwater snail, Planorbarius corneus. The present study reveals that ACTH and CRF affect the release of biogenic amines. Hemocytes from P. corneus hemolymph incubated in vitro with ACTH for 15, 30, and 45 min released epinephrine, norepinephrine, and dopamine. The greatest release occurred after 15 min, while after 45 min the values were similar to those of the controls. Similar incubations with CRF also provoked a release of biogenic amines, this being mainly mediated by the release of endogenous ACTH. These data suggest that (i) ACTH and CRF provoke the release of biogenic amines; (ii) there is a direct relationship between CRF, ACTH, and biogenic amines, with the hemocytes as the target; (iii) exogenous ACTH can mimic an ancestral type of stress response; (iv) the major pathway of the stress response in P. corneus is mediated by a CRF-ACTH-biogenic amine axis. These data should help to unravel part of the complex molecular signaling mechanisms involved in the physiological/endocrinological reaction of invertebrate organisms to stress, and suggest that a stress response unexpectedly similar to that present in mammalian cells is detectable in invertebrates.

Adrenocorticotropic Hormone↗