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At least 865 records · Page 48Linked to original sources
PubMed1996

Effect of fenfluramine on episodic ACTH and cortisol secretion.

OBJECTIVE: The central serotoninergic system is known to modulate the activity of the hypothalamic-pituitary-adrenal axis, but the effect of fenfluramine, a serotonin reuptake inhibitor, on ACTH and cortisol secretion is not well understood. We have therefore evaluated its effects on the hypothalamic-pituitary-adrenal axis in healthy controls. DESIGN: Episodic secretion of ACTH and cortisol was investigated in 6 healthy volunteers under basal conditions and again during treatment with 20 and 60 mg fenfluramine given orally every 8 hours. On all occasions blood samples were obtained at 10-minute intervals for 24 hours and the mode of hormone secretion was analysed by three different methods (PULSAR, CLUSTER, DESADE). In addition ACTH and cortisol responses to CRH were tested at the end of the sampling period. RESULTS: At the lower dose fenfluramine had no effect on ACTH and cortisol secretion. At the higher dose a significant increase of mean plasma ACTH (+85%) and cortisol (+129%) levels as well as of urinary free cortisol secretion (+44%) was observed. Fenfluramine did not modulate the frequency, but increased the amplitudes of ACTH and cortisol secretory episodes. ACTH and cortisol responses to CRH injection remained unchanged. Maximum plasma levels of d-fenfluramine and d-norfenfluramine were documented 2-4 hours after the ingestion of the drug. CONCLUSION: Fenfluramine stimulates the activity of the hypothalamic-pituitary-adrenal axis at a suprapituitary level by modulating the amplitude of ACTH and cortisol secretory bursts.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Aldosterone responses to ACTH during hypoxia in conscious rats.

This study examined the aldosterone response to physiological ACTH infusion (4 ng/kg per min) and pharmacological ACTH injection (1.8 microgram) in conscious Long-Evans rats at 42 h of normoxia (21% O2) or hypoxia (10% O2). Hypoxia per se (no exogenous ACTH) significantly decreased control aldosterone levels despite elevated endogenous plasma ACTH). Hypoxia attenuated the aldosterone responses to ACTH infusion but not to ACTH injection. It was concluded that hypoxia attenuates aldosterone responses to small increases in ACTH, and large increases in ACTH can override this apparent decrease in adrenocortical sensitivity.

Adrenocorticotropic Hormone↗
PubMed1989

Progesterone antagonizes development but not maintenance of ACTH-induced hypertension in sheep.

1. This study investigated the effect of progesterone, which, under certain circumstances, can antagonize both the mineralocorticoid and glucocorticoid activities of steroid hormones, on the development and maintenance of adrenocorticotrophic hormone (ACTH)-induced hypertension in conscious sheep. 2. Progesterone (500 mg/day) alone, for 5 days, had no effect on blood pressure, but increased urinary Na excretion by 38 +/- 10 mmol/day (P less than 0.05) during the first 24 h. 3. Infusion of ACTH (5 micrograms/kg per day), alone, for 3 days, increased arterial pressure by 21 +/- 2 mmHg (P less than 0.001) associated with hypernatraemia, hypokalaemia, urinary Na retention, and increased fasting plasma glucose concentration. 4. Progesterone (500 mg/day) concurrently with ACTH blocked the rise in mean arterial pressure and the mineralocorticoid (urinary Na retention) but not the glucocorticoid (increase in plasma glucose concentration) effects associated with ACTH administration. 5. Progesterone (500 and 1000 mg/day) failed to reverse the hypertension and hypokalaemia in sheep pretreated for 3 days with ACTH. 6. Thus, progesterone blocked the onset but did not affect established ACTH hypertension. The mechanism by which progesterone blocked the development of ACTH hypertension appears to be related to the ability of progesterone to block the essential mineralocorticoid component of the adrenocortical steroids involved in the development of ACTH hypertension.

Adrenocorticotropic Hormone↗
PubMed1990

Naloxone-induced ACTH release in man is inhibited by clonidine.

1. Adrenergic mechanisms play an important role in regulation of ACTH release. We used the alpha 2-adrenergic agonist, clonidine, as a central nervous system inhibitor of ACTH release to see if it would alter naloxone-induced ACTH secretion in normal human volunteers. 2. There was a significant blunting of the mean peak level of ACTH and the mean peak change of ACTH from basal as well as the area under the ACTH-time curve when clonidine was given prior to naloxone. 3. We conclude that clonidine, by blocking central noradrenergic pathways, which stimulate corticotropin-releasing hormone secretion, inhibits naloxone-induced ACTH secretion. This suggests that naloxone causes ACTH release through these same central noradrenergic pathways.

Administration, Oral↗
PubMed1993

The effect of non-depot ACTH(1-24) on infantile spasms.

However, side-effects such as severe infections, hypertension and electrolyte imbalance have been found, assumed to be related to hypercortisolism induced by chronic ACTH treatment. The authors treated 18 patients with infantile spasms with non-depot ACTH(1-24). The therapeutic effect of non-depot ACTH was comparable to that of depot ACTH, with no severe bacterial infection or sepsis. The incidence of hypertension was significantly lower in the non-depot ACTH group, and persistent hypercortisolaemia was not found. Non-depot ACTH(1-24) appears to be as effective as ACTH(1-24) depot therapy in the treatment of infantile spasms, and its side-effects are mild. It would appear that the effect of non-depot ACTH is not mediated by hypercortisolism, but by a direct neurotropic effect on the brain.

Adrenal Glands↗
PubMed1988

Facilitation of noradrenaline release from sympathetic nerves through activation of ACTH receptors, beta-adrenoceptors and angiotensin II receptors.

1. In rabbit pulmonary artery and left atrial strips previously incubated with [3H]-noradrenaline, the active fragment of adrenocorticotropic hormone (ACTH 1-24, 0.1 microM) significantly enhanced the stimulation-induced (S-I) outflow of radioactivity when a cocktail containing corticosterone (40 microM), cocaine (30 microM) and propranolol (4 microM) was present, but not in the absence of these drugs. In rabbit pulmonary artery a facilitatory effect of ACTH 1-24 (0.1 microM) was also observed when only cocaine (30 microM) was present. 2. ACTH 1-24 (0.1 microM) did not affect the S-I outflow of radioactivity from rat atria, rat pulmonary artery or guinea-pig pulmonary artery, either in the presence or in the absence of the cocktail containing corticosterone (40 microM), cocaine (30 microM) and propranolol (4 microM). These results suggest that the presence of facilitatory prejunctional ACTH receptors may be restricted to rabbit sympathetic nerve endings. 3. Angiotensin II (0.01 microM), but not isoprenaline (0.1 microM) or ACTH 1-24 (0.1 microM), significantly enhanced the S-I outflow of radioactivity from rabbit pulmonary artery. In the presence of phentolamine (1 microM) to block inhibitory alpha 2-adrenoceptors, the facilitatory effect of angiotensin II (0.01 microM) was significantly enhanced, and a significant facilitatory effect of isoprenaline (0.1 microM) and of ACTH 1-24 (0.1 microM) was then revealed. These results suggest that feedback inhibition of noradrenaline release, mediated through the prejunctional alpha 2-adrenoceptor mechanism, buffers increases in noradrenaline release during activation of facilitatory prejunctional receptors. 4. In rabbit pulmonary artery, two concentrations of 8-Br-cyclic AMP, (270 or 540 microM), enhanced the S-I outflow of radioactivity in the presence of phentolamine (1 microM) to a similar extent. In the presence of 8-Br-cyclic AMP (270 microM) and phentolamine, the facilitatory effects of isoprenaline (0.1 microM) and of ACTH,24 (0.1 microM) were blocked, whereas that of angiotensin II (0.01 microM) was not changed. These results suggest that both prejunctional beta-adrenoceptors and ACTH receptors enhance noradrenaline release by generating cyclic AMP. The mechanism by which angiotensin II facilitates noradrenaline release is probably independent of the cyclic AMP second messenger pathway.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

ACTH release induced in rats by noradrenaline is mediated by prostaglandin E2.

1. We investigated the involvement of prostaglandin E2 in the development of the adrenocorticotrophic hormone (ACTH) response induced by noradrenaline (NA) in rats. 2. Intravenous (i.v.) injection of NA produced dose-dependent increases in the plasma concentration of ACTH and prostaglandin E2. However, pre-treatment with systemic administration of indomethacin, an inhibitor of prostaglandin synthesis, significantly suppressed this increase in plasma ACTH. 3. The i.v. injection of prostaglandin E2 significantly increased the plasma concentration of ACTH in a dose-dependent manner. In contrast, ACTH responses induced by the i.v. injection of prostaglandin E2 were significantly suppressed by systemic pre-treatment with anti-corticotrophin-releasing factor antibody (anti-CRF), although the plasma level of ACTH still increased in comparison to the basal level. 4. These results suggest that NA-stimulated prostaglandin release is involved in the ACTH response induced by NA. In addition, it is likely that CRF may be responsible for a portion of the ACTH response induced by i.v. injection of prostaglandin E2.

Adrenocorticotropic Hormone↗
PubMed1979

Effect of ACTH on the aldosterone response to potassium in sheep with adrenal transplants.

The importance of physiological ACTH stimulation in maintaining the response of aldosterone secretion to potassium was studied in 5 conscious sheep with cervical adrenal autotransplants. Endogenous ACTH secretion was suppressed by dexamethasone. Constant local infusions of potassium that raised adrenal venous plasma by 2 mmol/l increased aldosterone secretion from 3 +/- 1 ng/min (mean +/- SE) to levels of 50 +/- 13 ng/min at 30 min, after which secretion fell to 14 +/- 6 ng/min at 230 min. Addition of submaximal ACTH (0.04 - 0.10 mU/min) to potassium infusions produced similar responses at 0--130 min, but aldosterone secretion increased at 130--190 min and was more sustained (40 +/- 9 ng/min at 230 min; P less than 0.05). Infusions of submaximal ACTH alone did not significantly increase aldosterone secretion above basal levels. Infusions of maximal ACTH (16.6 mU/min) produced higher aldosterone secretion in the group given ACTH replacement. These results show that the aldosterone response to potassium is phasic and poorly sustained in the absence of ACTH. Responsiveness can be restored by doses of ACTH insufficient alone to stimulate aldosterone secretion.

Adrenal Cortex↗
PubMed1988

Effects of CRF and ANG II on ACTH and vasopressin release in conscious dogs.

The aim of the present study was to examine the effects of corticotropin-releasing factor (CRF) in conscious dogs and to determine whether the stimulation of adrenocorticotropic hormone (ACTH) release by angiotensin II (ANG II) results from potentiation of the action of CRF. In addition, the possible role of CRF in the stimulation of vasopressin released by ANG II was investigated. The following experiments were performed: 1) intravenous saline infusion; 2) ANG II (10 ng.kg-1.min-1) alone; 3) vasopressin (1 ng.kg-1.min-1) alone; 4) CRF (0.001, 0.01, or 0.1 microgram/kg iv) bolus; 5) vasopressin (1 ng.kg-1.min-1) and CRF (0.1 microgram/kg) together; 6) CRF (0.001, 0.01, or 0.1 microgram/kg) and ANG II (10 ng.kg-1.min-1) together; 7) ANG II (10 ng.kg-1.min-1) followed 15 min later with CRF (0.001, 0.01, or 0.1 microgram/kg). Each dose of CRF was tested on a different day. Infusion of ANG II alone stimulated the release of ACTH, cortisol, and vasopressin. Administration of CRF produced dose-dependent increases in plasma ACTH and cortisol concentrations, and the highest dose of CRF increased plasma vasopressin concentration. CRF given together with ANG II did not potentiate the stimulation of ACTH release by CRF. Vasopressin at the dose tested did not stimulate ACTH release but potentiated the ACTH response to CRF. ANG II stimulated vasopressin release but did not potentiate the AVP response to CRF. These results show that, in conscious dogs, ANG II and CRF each increase plasma ACTH concentration and that the ACTH response to CRF is potentiated by vasopressin but not by ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1988

Steroid inhibition of canine ACTH: in vivo evidence for feedback at the corticotrope.

We infused submaximal feedback doses of either dexamethasone (DEX; 0.1 microgram.kg-1.min-1) or corticosterone and cortisol (B+F; 1.5 micrograms.kg-1.min-1) intravenously for 40 min into conscious dogs and measured the adrenocorticotropic hormone (ACTH) responses to hypoglycemia induced by insulin (0.1 U/kg) or to ovine corticotropin-releasing factor (oCRF; 1 microgram/kg); both agents were injected at 120 min. The dose of DEX was chosen to produce suppression of the ACTH response to oCRF equivalent to that produced by B+F. The purpose of the study was to determine 1) whether CRF- and hypoglycemia-induced ACTH secretion are equally inhibited by glucocorticoid treatment and 2) whether DEX and B+F have differential effects in the inhibition of stress-induced ACTH secretion. We found that peak ACTH responses to hypoglycemia and CRF were equally inhibited by DEX (36 +/- 6 and 52 +/- 9%, respectively). The peak ACTH responses to hypoglycemia and CRF were also equally inhibited after B+F infusion (45 +/- 13 and 65 +/- 5%, respectively). There was no significant interaction between the steroid administered and the stimulus given in controlling the ACTH response (by 2-way analysis of variance). The results suggest that pituitary feedback is of primary importance in suppression of canine ACTH secretion by delayed feedback and that the natural and synthetic steroids both act at this site.

Adrenocorticotropic Hormone↗
PubMed2002

Adrenocortical responses to ACTH in neonatal rats: effect of hypoxia from birth on corticosterone, StAR, and PBR.

The adrenocortical response to hypoxia may be a critical component of the adaptation to this common neonatal stress. Little is known about adrenal function in vivo in hypoxic neonates. The purpose of this study was to evaluate adrenocortical responses to ACTH in suckling rat pups exposed to hypoxia from birth to 5-7 days of age compared with normoxic controls. We also evaluated potential cellular controllers of steroidogenic function in situ. In 7-day-old pups at 0800, hypoxia from birth resulted in increased basal (12.2 +/- 1.4 ng/ml; n = 12) and ACTH-stimulated (94.0 +/- 9.4 ng/ml; n = 14) corticosterone levels compared with normoxic controls (basal = 8.3 +/- 0.5 ng/ml; n = 11; stimulated = 51.3 +/- 3.8 ng/ml; n = 8). This augmentation occurred despite no significant difference in plasma ACTH levels in normoxic vs. hypoxic pups before (85 +/- 4 vs. 78 +/- 8 pg/ml) or after (481 +/- 73 vs. 498 +/- 52 pg/ml) porcine ACTH injection (20 microg/kg). This effect was similar in the afternoon at 6 days of age and even greater at 5 days of age at 0800. The aldosterone response to ACTH was not augmented by exposure to hypoxia from birth. Adrenocortical hypoxia-inducible factor (HIF)-1alpha mRNA was undetectable by RT-PCR. Steroidogenic acute regulatory (StAR) protein in adrenal subcapsules (zona fasciculata/reticularis) was augmented by exposure to hypoxia; this effect was greatest at 5 days of age. Peripheral-type benzodiazepine receptor (PBR) protein was also increased at 6 and 7 days of age in pups exposed to hypoxia from birth. We conclude that hypoxia from birth results in an augmentation of the corticosterone but not aldosterone response to ACTH. This effect appears to be mediated at least in part by an increase in controllers of mitochondrial cholesterol transport (StAR and PBR) and to occur independently of measurable changes in endogenous plasma ACTH. The augmentation of the corticosterone response to acute increases in ACTH in hypoxic pups is likely to be an important component of the overall physiological adaptation to hypoxia in the neonate.

Adrenal Glands↗
PubMed1988

Control of canine ACTH by corticosteroids: interaction between dose and time.

These experiments were designed to test for interactions between dose and time of administration of steroids in control of adrenocorticotropin hormone (ACTH). Five dogs were infused for 30 min with cortisol and corticosterone in a 2:1 ratio at a total rate of 1.5 or 3.0 micrograms.kg-1.min-1 beginning 120, 90, 60, 30, or 0 min before injection of insulin (0.5 U/kg). The infusions increased total plasma corticosteroids to approximately 50 or 80 ng/ml. Inhibition of basal ACTH occurred when infusion of steroid at either rate began greater than or equal to 60 min earlier. The degree of inhibition of stimulated ACTH was dependent on both steroid dose and timing of steroid infusion relative to the stimulus. Increasing corticosteroids to 50 ng/ml reduced the ACTH response to hypoglycemia if the infusion began 30 min, but not 60, 90, or 120 min earlier. Increasing corticosteroids to 80 ng/ml inhibited the response if the infusion began 120 or 60 min before injection of insulin. The data suggest that 1) inhibition of stimulated ACTH required less than or equal to 30 min to appear; 2) the duration of corticosteroid feedback is steroid-dose related; 3) basal ACTH secretion is more sensitive than stimulated ACTH to steroid inhibition; 4) small increments in plasma corticosteroids over short periods of time can inhibit canine ACTH.

Adrenal Cortex Hormones↗
PubMed1988

Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats.

The control of aldosterone secretion may be altered during acute changes in arterial blood gases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 +/- 2.0 ng.ml-1.h-1), ACTH (96 +/- 32 pg/ml), and ALDO (10 +/- 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 +/- 69 pg/ml) and ALDO (to 33 +/- 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 +/- 14 pg/ml) and ALDO (to 30 +/- 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 +/- 2 ng.ml-1.h-1), ACTH (to 397 +/- 114 pg/ml), and ALDO (to 41 +/- 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (less than 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (Po2 approximately 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.

Acute Disease↗
PubMed1988

Immune activation and psychoneurogenic stress modulate corticosterone-releasing effects of lymphokines and ACTH.

Possible modulatory effects of psychoneurogenic stress and endotoxin-induced immune activation on the in vitro corticosterone-releasing effects of lymphokine-containing supernatants (LCS) and adrenocorticotropic hormone (ACTH) were studied in rats. We have found that activation of the immune system by endotoxin increases the in vitro sensitivity of the adrenocortical cells to LCS and ACTH. In addition, we found that psychoneurogenic stress not only produced an increase of in vitro adrenal sensitivity to ACTH, but it also enhanced the release of corticosterone after perfusion of LCS. A synergistic interaction between ACTH and LCS was observed in all experimental groups of animals studied. An increased adrenal sensitivity to LCS and ACTH after stress or immune activation might have a functional significance, since the adrenal cortex is a major site in the response of the organism to alterations in the homeostatic balance. On the other hand, the temporal pattern of in vitro corticosterone release after LCS was different in all groups under study compared with that observed after ACTH challenge. LCS elicited a more rapid corticosterone response that lasted for a shorter time than after giving ACTH. These latter results suggest that different mechanisms may underlie the effects of LCS and ACTH on adrenal corticosteroidogenesis. In conclusion, the present findings further reinforce the existence of possible physiologically relevant interactions between the immune system and the pituitary-adrenal axis.

Adrenal Glands↗
PubMed1989

ACTH-induced hypertension in rats: fact or artifact?

Evidence from numerous laboratories has shown that administration of adrenocorticotropic hormone (ACTH) to rats produces hypertension within 5 days. However, the analysis of blood pressure in these studies was by the tail-cuff technique, an acute and indirect approach. We have now administered ACTH, via a subcutaneous depot injection (5 or 10 U/day for 9 days), to chronically instrumented rats maintained in metabolic cages. Although tail-cuff measurements of arterial pressure indicated that the ACTH treatment produced hypertension, this was not confirmed by direct 24-h measurements of mean arterial pressure. There was no effect of ACTH on 24-h heart rate throughout the treatment period compared with saline-injected controls. We also examined coefficient of variation of all our measurements. None of the factors was altered by ACTH administration. However, ACTH treatment did produce a diuretic effect, further confirming previous work and providing renal, in addition to cardiovascular, evidence for the bioavailability of the ACTH depot. These results demonstrate that chronic ACTH treatment does not produce a true hypertensive state in rats but rather may enhance the cardiovascular response to the stress of the indirect arterial pressure measurement technique.

Adrenocorticotropic Hormone↗
PubMed2000

Significant gene expression of insulin-like growth factor II and proliferating cell nuclear antigen in a rapidly growing recurrent pituitary acth-secreting adenoma.

BACKGROUND: We quantified the expression of various growth-related factors in an adrenocorticotropic hormone (ACTH)-secreting adenoma that had recurred very rapidly as invasive macroadenoma. METHODS/RESULTS: A 43-year-old woman underwent successful transsphenoidal surgery for Cushing's disease. Seven years later, she was admitted to our ward for further endocrine examinations. In spite of a very high plasma ACTH level, the serum cortisol level was normal. Discrepancies between ACTH and cortisol levels were detected on the basis of diurnal rhythms, dexamethasone suppression tests, and corticotropin-releasing hormone test. The patient showed no clinical features of Cushing's disease. Magnetic resonance imaging of the pituitary showed an almost empty sella, and no microadenoma was found. These results, along with those of Sephadex column gel filtration and high-performance liquid chromatography of plasma-immunoreactive ACTH, suggested that the patient's residual corticotrophs secreted biologically inactive ACTH. Two years later, the patient suddenly developed diplopia and right abducens nerve palsy. She was slightly moonfaced and centrally obese. Her plasma ACTH and serum and urinary free cortisol levels were elevated, although discrepancies between ACTH and cortisol still existed. Magnetic resonance imaging revealed a large pituitary mass with suprasellar and cavernous sinus extensions. The tumor was excised, and the proopiomelanocortin gene and the expression of growth-related factors were analyzed. No mutations were found in the ACTH-coding region of the proopiomelanocortin gene. A significant expression of insulin-like growth factor II and proliferating cell nuclear antigen mRNAs was demonstrated. A high MIB-1 antibody labeling index was also detected in the adenoma tissue, suggesting high Ki-67 expression. CONCLUSION: These growth- and proliferation-related factors might be involved in the rapid growth and aggressiveness of this patient's pituitary adenoma.

Adenoma↗
PubMed1998

Differential sensitivity to ACTH, but not stress, in two sources of outbred Sprague-Dawley rats.

Adrenocorticotropic hormone (ACTH) is the major regulator of adrenocortical steroidogenesis in mammals. By comparing the sensitivity to ACTH of isolated adrenocortical cells from two sources of the same strain (Sprague-Dawley, SD) of outbred rats, we have identified a source of rat with low sensitivity to ACTH in vitro. Cells isolated from Holtzman SD rats had a high sensitivity to ACTH (minimal effective concentration 50 pg/ml), whereas Taconic SD rats had a low sensitivity (minimal effective concentration 250 pg/ml; maximal steroidogenesis < 50% of Holtzman cells). The responsiveness to analogues of cyclic adenosine monophosphate and cholesterol was also significantly lower in Taconic SD rats. Taconic adrenals were smaller, had significantly more mitochondria per cell, but approximately 20% less total lipid droplet volume per cell. There was no difference in latency to ACTH in vitro; however, steroidogenesis plateaued in Taconic cells after 25 min, while Holtzman cells secreted corticosterone almost linearly for at least 120 min. By contrast, the cyclic adenosine monophosphate secretion increased at the same rate for at least 120 min in cells from both sources. There were no differences between cells from the two sources in immunoreactive steroidogenic enzyme content. In vivo, the magnitude of the ACTH and corticosterone responses to two types of stress were similar in both sources. The thymus glands of Holtzman rats were significantly larger than those of Taconic rats. It is concluded that: (1) reduced sensitivity to ACTH in vitro in Taconic SD rats results from differences in the later stages of the steroidogenic pathway; (2) factors in addition to ACTH are required for maximal steroidogenesis in Taconic SD rats: (3) a comparison of the steroidogenic pathways in adrenal cells from these two sources of outbred rats should be useful in further delineating the relative importance of putative intracellular signalling mechanisms involved in initiation and maintenance of steroidogenesis, and (4) these data suggest that different sources of the same strain of rats sufficiently diverge over time to become separate strains ('substrains'). Overreliance on a single source of laboratory rodent may obscure natural variability in endocrine responses to stress and provide a misleading indication of homogeneity of responses.

Adrenal Cortex↗
PubMed1977

Pars intermedia ACTH and MSH content: effect of adrenalectomy, gonadectomy and a neurotropic (noise) stress.

Pars intermedia (PI) ACTH and melanocyte-stimulating hormone (MSH) content and pars distalis (PD) ACTH concentration were measured following 3 experimentally induced 'perturbations'. The feedback-induced increase in ACTH release following adrenalectomy is not accompanied by a change in PI ACTH and MSH contents, while the feedback-induced increase in gonadotropin secretion following gonadectomy is associated with significant changes in PI ACTH and MSH contents. A well-defined neurotropic (noise) stressor resulted in significant increases in PI ACTH and MSH. A striking finding in all of the studies was a positive correlation between PI ACTH and MSH contents. We conclude that PI ACTH and MSH secretion are altered with feedback-induced alterations in gonadotropin secretion and with neurotropic stressors.

Adrenal Glands↗