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PubMed1990

Corticotropin, cortisol and beta-endorphin responses to the human corticotropin-releasing hormone during melancholia and after unilateral electroconvulsive therapy.

Previous research in neuroendocrinology has evidenced that hyperactivity of the hypothalamic-pituitary-adrenal axis (HPA) depends on hypersecretion of corticotropin-releasing hormone (CRH). The aim of this study was to investigate the activity of HPA before and after recovery in depressed patients treated with electroconvulsive therapy (ECT). An h-CRH-stimulation test was performed on 2 occasions with examination of the HPA axis before ECT treatment during episodes of major depressive disorders with melancholia, and during the recovery phase after treatment. The results showed that patients during depression had significantly higher plasma levels of cortisol at 15 and 30 min after h-CRH-administration than after recovery. Depressed patients had significantly higher plasma levels of beta-endorphin 30 min after h-CRH-stimulation. The results are in agreement with previous studies, which have shown hypercortisolemia during depression. A possible hypersecretion of CRH may explain the effect on cortisol and beta-endorphin. No significant differences were found between cumulative responses of corticotropin, cortisol and beta-endorphin, calculated as the areas under the concentration curves.

Adrenocorticotropic Hormone↗
PubMed1993

Release of corticotropin after administration of corticotropin-releasing hormone in depressed patients in relation to the dexamethasone suppression test.

The possible hypersecretion involvement of corticotropin-releasing hormone (CRH) in the pathophysiology of hypothalamic-pituitary-adrenocortical axis disturbances in patients with major depressive episode and with an abnormal dexamethasone suppression test (DST) was investigated. The corticotropin (ACTH) and cortisol response to the injection of 45 micrograms of synthetic human CRH at 1630 were analyzed in 24 inpatients with normal (suppressors) or abnormal (nonsuppressors) DST. The outcome of the DST was analyzed using 3 cut-off points for the cortisol levels. The clinical assessments included two rating scales. The results showed that nonsuppressors had a significantly lower ACTH response to CRH stimulation than suppressors at all cut-off points (calculated as net area under the curve and as the difference between the peak and the baseline level) despite no significant differences in the severity of depression.

Adrenocorticotropic Hormone↗
PubMed1996

Changes in late auditory evoked potentials induced by corticotropin-releasing hormone and corticotropin fragment 4-9 in male controls.

In order to investigate influences of corticotropin-releasing hormone (CRH) and corticotropin fragment (adrenocorticotropic hormone, ACTH, 4-9) on auditory perception processes, 10 subjects received either a placebo (sodium chloride 0.9%), CRH (100 micrograms) or ACTH 4-9 (Hoe 427, 300 micrograms) intravenously on different days. Late auditory evoked potentials (AEP) were computed and further analyzed using the brain electric source analysis method. As expected, CRH administration was followed by a rise in plasma cortisol and ACTH concentrations, whereas the injection of the ACTH 4-9 fragment did not alter plasma cortisol concentrations. In contrast to these different hormonal responses, both CRH and ACTH 4-9 modulated AEP in a similar manner, differing in quantity rather than in quality. The changes in AEP after the administration of ACTH 4-9 were most likely induced by a direct CNS action, whereas for the CRH effects, an indirect mechanism throughout the release of endogenous ACTH must be considered.

Adrenocorticotropic Hormone↗
PubMed1991

Circadian patterns of plasma immunoreactive corticotropin, beta-endorphin, corticosterone and prolactin after immunoneutralization of corticotropin-releasing hormone.

To study the role of corticotropin-releasing hormone (CRH) in the circadian rhythm of circulating corticotropin (ACTH), beta-endorphin (beta-END), corticosterone, and prolactin (PRL), we measured the effects of CRH immunoneutralization over a 24-hour period in chronically cannulated, conscious, freely moving, male Sprague-Dawley rats, maintained at a constant light-dark cycle. Blood samples were collected in the morning (08.00 h), at noon (12.00 h), and in the evening (18.00 h) on the day of treatment, and in the morning (08.00 h) of the next day. Hyperimmune rabbit serum raised against rat CRH (1.0 ml/rat, i.v.) or normal rabbit serum (NRS, 1.0 ml/rat, i.v.) was administered at 08.00 h, immediately after the first blood sample had been collected. CRH immunoneutralization caused no significant decreases in circulating immunoreactive ACTH, beta-END and corticosterone plasma levels at noon, but abolished the evening rises of these hormones. PRL levels were not significantly different between the groups at any time point measured. To compare the effects of CRH immunoneutralization to those of glucocorticoid negative feedback, we measured the effects of dexamethasone (0.5 mg/kg, i.v. at 08.00 h) on the above parameters. ACTH and beta-END concentrations were significantly decreased, and corticosterone and PRL levels were markedly suppressed after glucocorticoid administration both at 12.00 and 18.00 h. However, 24 h after the administration of dexamethasone, PRL concentrations were elevated despite persistently low corticosterone levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

Cerebrospinal fluid concentrations of corticotropin-releasing hormone (CRH) and corticotropin (ACTH) are reduced in patients with Alzheimer's disease.

We examined corticotropin-releasing hormone-like immunoreactivity (CRH-LI) and corticotropin (ACTH) levels in the CSF of 33 patients with presumptive Alzheimer's disease (AD) and 13 healthy, age-matched controls. The mean CRH-LI and ACTH levels of the AD patients were significantly less than controls. Despite these reductions, none of the patients had evidence of pituitary-adrenal dysfunction. A disorder of extrahypothalamic CRH may be involved in the pathophysiology of AD.

Adrenocorticotropic Hormone↗
PubMed1990

Somatostatin analogue (SMS 201-995) decreases plasma levels of corticotropin (ACTH) and corticotropin-releasing hormone in a patient with ectopic ACTH-producing tumors.

Effects of long-acting somatostain analogue (SMS 201-995) on plasma corticotropin (ACTH) and corticotropin-releasing hormone (CRH) levels were studied in a patient (63-year-old woman) with ectopic ACTH-producing tumors associated with type I multiple endocrine neoplasia (MEN-I). The patient had undergone bilateral adrenalectomy. Plasma CRH, as well as plasma ACTH, beta-endorphin and alpha-MSH, increased. The hormone levels were dramatically decreased by acute administration of SMS 201-995. Moderately higher doses of dexamethasone (0.05 or 0.1 mg/kg a day) did not decrease plasma CRH or ACTH. An extremely high dose of dexamethasone (0.2 mg/kg a day), however, decreased plasma ACTH, but failed to decrease plasma CRH. Acute administration of SMS 201-995 further lowered the level of plasma ACTH even in this condition. In addition to the decrease in ACTH, SMS 201-995 decreased plasma CRH. Chronic administration of SMS 201-995 continuously decreased plasma CRH, ACTH and beta-endorphin. The decrease in these hormone concentrations accompanied the disappearance of hyperpigmentation. These results suggested that SMS 201-995 inhibits hypersecretion not only of ACTH but also of CRH, and that the agent is therapeutically useful in normalizing the hypersecretion of these hormones.

ACTH Syndrome, Ectopic↗
PubMed2001

Corticotropin (ACTH) acts directly on amygdala neurons to down-regulate corticotropin-releasing hormone gene expression.

The hormone corticotropin (ACTH) is employed as therapy for diverse neurological disorders, but the mechanisms for its efficacy remain unknown. ACTH promotes the release of adrenal steroids (glucocorticoids), and most ACTH effects on the central nervous system (CNS) have been attributed to activation of glucocorticoid receptors. However, in several human disorders, ACTH has therapeutic actions that differ qualitatively or quantitatively from those of steroids. This study tested the hypothesis that ACTH directly influences limbic neurons via the recently characterized melanocortin receptors and focused on the effects of ACTH on the expression of corticotropin-releasing hormone (CRH), a neuropeptide involved in neuroimmune functions and in certain developmental seizures. The results demonstrated that ACTH potently reduced CRH expression in amygdala neurons. This down-regulation was not abolished by experimental elimination of steroids or by blocking their receptors and was reproduced by a centrally administered ACTH fragment that does not promote steroid release. Importantly, selective blocking of melanocortin receptors prevented ACTH-induced down-regulation of CRH expression. Taken together, these data indicate that ACTH activates central melanocortin receptors to modulate CRH gene expression in amygdala, supporting the notion that direct, steroid-independent actions of ACTH may account for some of its established clinical effects on the CNS.

Adrenocorticotropic Hormone↗
PubMed1980

Release of corticotropin and corticotropin-releasing factors from rat posterior pituitary in vitro.

Electrical stimulation of rat posterior lobes in vitro inhibited bioactive corticotropin (ACTH) release from the intermediate lobe and promoted the release of corticotropin-releasing factor(s) (CRF). Both effects were calcium dependent. Released posterior lobe CRF was inactivated by thioglycolate, and the CRF activity could be accounted for by vasopressin. Results suggest strongly that vasopressin is the predominant CRF released from neurohypophysial axons, and that intermediate lobe ACTH release is submitted to an inhibitory control.

Adrenocorticotropic Hormone↗
PubMed1983

Mechanisms of action of corticotropin-releasing factor and other regulators of corticotropin release in rat pituitary cells.

The role of cyclic AMP in the stimulation of corticotropin (ACTH) release by corticotropin-releasing factor (CRF), angiotensin II (AII), vasopressin (VP), and norepinephrine (NE) was examined in cultured rat anterior pituitary cells. Synthetic CRF rapidly stimulated cyclic AMP production, from 4- to 6-fold in 3 min to a maximum of 10- to 15-fold at 30 min. Stimulation of ACTH release by increasing concentrations of CRF was accompanied by a parallel increase in cyclic AMP formation, with ED50 values of 0.5 and 1.3 nM CRF for ACTH and cyclic AMP, respectively. A good correlation between cyclic AMP formation and ACTH release was also found when pituitary cells were incubated with the synthetic CRF(15-41) fragment, which displayed full agonist activity on both cyclic AMP and ACTH release with about 0.1% of the potency of the intact peptide. In contrast, the CRF(21-41) and CRF(36-41) fragments were completely inactive. The other regulators were less effective stimuli of ACTH release and caused either no change in cyclic AMP (AII and VP) or a 50% decrease in cyclic AMP (NE). Addition of the phosphodiesterase inhibitor, methylisobutylxanthine, increased the sensitivity of the ACTH response to CRF but did not change the responses to AII, VP, and NE. In pituitary membranes, adenylate cyclase activity was stimulated by CRF in a dose-dependent manner with ED50 of 0.28 nM, indicating that the CRF-induced elevation of cyclic AMP production in intact pituitary cells is due to increased cyclic AMP biosynthesis. The intermediate role of cyclic AMP in the stimulation of ACTH release by CRF was further indicated by the dose-related increase in cyclic AMP-dependent protein kinase activity in pituitary cells stimulated by CRF with ED50 of 1.1 nM. These data demonstrate that the action of CRF on ACTH release is mediated by the adenylate cyclase-protein kinase pathway and that the sequence requirement for bioactivity includes the COOH-terminal 27 amino acid residues of the molecule. The other recognized regulators of ACTH release are less effective stimuli than CRF and do not exert their actions on the corticotroph through cyclic AMP-dependent mechanisms.

Adrenocorticotropic Hormone↗
PubMed1981

Quantitative analysis of the lipid-mobilizing effects of corticotropin, beta 1-24--corticotropin (tetracosactide) and isoprenaline in older rats and rabbits.

The lipid mobilizing effects of corticotropin (ACTH), beta 1-24-corticotropin-tetracosactide (TCA) and isoprenaline (ISO) were studied in parallel experiments in older rabbits (six months, weight 3.5 kg) and rats (age 75-85 days, weight 275 g) in vitro. The results were analysed quantitatively. Compared with the effect in younger rats the lipid mobilizing action of ISO in older animals does not differ. The same applies to the very low ISO lipolytic potency in rabbits. The ACTH intrinsic activity and affinity decrease in aging rabbits, but not in aging rats. At the concentration 1 x 10(-9) mol/l of TCA 35% of its maximum effect is reached in rabbits and almost the maximum in rats. In comparison with the maximum response to ACTH the maximum of TCA is two times higher in rabbits whereas in rats it reaches only 80% of the ACTH maximum. The order of the intrinsic activities is in older rats and rabbits different: ISO much greater than ACTH greater than TCA (1.00:0.81:0.64) in rats and TCA greater than ACTH greater than ISO (1.00:0.53:0.31) in rabbits. The affinity relations TCA greater than ISO greater than ACTH are identical in both species with the ratios of ACTH:ISO:TCA = 1:50:1740 in rats and 1:34:915 in rabbits. TCA exerts the strongest lipolytic potency in rats which is 5.5 times greater than in rabbits. On the contrary the intrinsic activity of TCA in rabbits is the highest. In older rabbits the ACTH adipokinetic intrinsic activity and affinity decrease faster than those in ISO. The species differences especially in relation to ISO also remain preserved in older animals and this applies to the TCA lipolytic effects, which in turn do not seem to change with aging as much as the effects of ACTH. When evaluating the species differences or the sensitivity changes connected with aging in the action of lipolytic drugs, the intrinsic activity and affinity should be considered separately.

Adipose Tissue↗
PubMed2001

Corticotropin-releasing hormone signaling in synovial tissue from patients with early inflammatory arthritis is mediated by the type 1 alpha corticotropin-releasing hormone receptor.

OBJECTIVE: Elevated levels of corticotropin-releasing hormone (CRH) are produced locally in inflamed human synovial tissue, and previous observations indicate a role for CRH in the pathogenesis of inflammatory joint disease. To further elucidate the biologic role of CRH at peripheral sites, we examined the expression of known CRH receptor subtypes in inflamed human synovium and compared the expression patterns in normal synovium. METHODS: Immunohistochemical analysis was used to confirm enhanced expression of specific CRH receptor subtypes in rheumatoid arthritis (RA) and psoriatic arthritis (PsA) synovium. Immunofluorescence double-labeling was used to further characterize CRH receptor-expressing cells. Reverse transcriptase-polymerase chain reaction analysis was performed to examine CRH receptor subtype messenger RNA (mRNA) expression in RA, PsA, and normal synovial tissue. In addition, CRH receptor expression was examined in isolated synovial endothelial cells and synoviocytes. RESULTS: Selective up-regulation of CRH receptors in inflamed synovial tissue indicated that CRH functions locally, in an autocrine/paracrine receptor-mediated manner. Immunoreactive CRH receptor type 1 (CRH-R1) was expressed abundantly on vascular endothelial cells and discrete perivascular cell populations, identified as mast cells. In all samples of inflamed synovium studied, CRH-R1alpha mRNA was detected; however, we were unable to identify CRH-R1beta or any CRH-R2 isoforms in samples from the same cohort of, patients. CRH receptor subtype expression in separated synovial cell populations revealed a pattern of staining similar to that seen in vivo. In contrast, neither CRH receptor subtype was expressed in normal synovial tissue. CONCLUSION: Our findings suggest that CRH signaling, via CRH-R1alpha, may play a role in both the vascular changes and the pathologic mechanisms associated with joint inflammation in human arthritis.

Arthritis, Psoriatic↗
PubMed1996

[D-Pro5]Corticotropin-releasing factor analogs as selective agonists at corticotropin-releasing factor receptors.

Corticotropin-releasing factor (CRF) acts on at least two types of CRF receptors. To search for selective CRF receptor agonists, 37 ovine CRF analogs, systematically substituted with D-amino acids, were tested for inhibitory activity on edema induced in the pentobarbital-anesthetized rat paw by heat (immersion in 58 degrees C water for 1 min). The activity of each analog, administered 21 nmol/kg i.v. 10 min before heat, was compared to published data on the analog's potency in stimulating adrenocorticotropin (ACTH) release from cultured rat pituitary cells. In general, a positive rank correlation was found between the anti-edema and neuroendocrine activities of these analogs, however, one outlier, [D-Pro5]ovine CRF, exhibited greater selectivity for anti-edema activity. The human/rat analog of [D-Pro5]CRF was synthesized and found to be equipotent to human/rat CRF for suppression of heat-edema. In cells transfected with two types of cloned CRF receptors, the intracellular cAMP response to [D-Pro5]human/rat CRF was equipotent to human/rat CRF in the heart-muscle CRF (CRF2 beta) receptor assay but was five times less potent than human/rat CRF in the pituitary-central nervous system CRF (CRF1) receptor assay. We conclude that changing residue Pro5 in the CRF molecule from a L- to a D-configuration confers selectivity by decreasing second messenger activation at the CRF1 receptor whilst retaining full potency at the CRF2 beta receptor.

Adrenocorticotropic Hormone↗
PubMed1995

Proopiomelanocortin, corticotropin releasing hormone and corticotropin releasing hormone receptor genes are expressed in human skin.

Evidence is provided that human skin, the largest body organ exposed to multiple stressors, expresses proopiomelanocortin (POMC), corticotropin releasing hormone (CRH) and CRH-receptor (CRHR) genes in vivo. In vitro studies show that POMC and CRHR mRNAs are transcribed in melanocytes, cells derived from the neural crest, and in keratinocytes, cells derived from the ectoderm. CRH mRNA is transcribed in cultured melanocytes but not in keratinocytes. It is proposed that an equivalent of the 'hypothalamus-pituitary axis' composed of the CRH-CRHR-POMC loop is conserved in mammalian skin.

Base Sequence↗
PubMed1999

Nitric oxide stimulates ACTH secretion and the transcription of the genes encoding for NGFI-B, corticotropin-releasing factor, corticotropin-releasing factor receptor type 1, and vasopressin in the hypothalamus of the intact rat.

We investigated the effect of the intracerebroventricular injection of the nitric oxide (NO) donor 3-morpholino-sydnonimine (SIN-1) on the release of adrenocorticotropin hormone (ACTH) and the neuronal response of hypothalamic neurons responsible for this release. Rats that were administered SIN-1 showed significant elevations in plasma ACTH levels, a response that was virtually abolished by antibodies against corticotropin-releasing factor (CRF) and significantly blunted by vasopressin (VP) antiserum. SIN-1 also upregulated heteronuclear (hn) transcripts for CRF and VP and messenger RNA (mRNA) levels for the immediate early gene NGFI-B and for CRF receptor type 1 (CRF-R(1)) in the parvocellular portion of the paraventricular nucleus (PVN) of the hypothalamus. Blockade of prostaglandin synthesis with ibuprofen did not alter the ACTH or the PVN response to SIN-1. The central nucleus of the amygdala and the supraoptic nucleus, regions that are involved in autonomic adjustments to altered cardiovascular activity, also responded to SIN-1 with elevated NGFI-B mRNA levels. However, the only change in mean arterial blood pressure caused by this NO donor was a transient and modest increase. To our knowledge, this is the first demonstration that in the intact rat NO stimulates the activity of PVN neurons that control the hypothalamic-pituitary-adrenal axis. It must be noted, however, that our results do not allow us to determine whether this effect was direct or mediated through PVN afferents. This study should help resolve the controversy generated by the use of isolated brain tissues to investigate the net effect of NO on hypothalamic peptide production.

Adrenocorticotropic Hormone↗
PubMed1996

Corticotropin-releasing factor and type 1 corticotropin-releasing factor receptor messenger RNAs in rat brain and pituitary during "binge"-pattern cocaine administration and chronic withdrawal.

Endogenous central corticotropin-releasing factor (CRF) may be involved in the neuroendocrine and behavioral responses to cocaine. In the present study, levels of CRF mRNA were measured in the hypothalamus and in several extrahypothalamic brain regions after different regimens of "binge"-pattern cocaine administration. Male Fischer rats were injected with saline or cocaine (15 mg/kg, 1 hr x 3/day) at the beginning of the light cycle, to approximate the manner in which cocaine is often abused by humans, both in terms of temporal pattern and in relation to circadian rhythm. Cocaine administered in this binge regimen produced time-dependent alterations of CRF mRNA levels in the hypothalamus. There was a significant increase in CRF mRNA levels on day 1, which returned to base-line levels on day 2, with elevated plasma corticosterone levels on both days. CRF receptor type 1 and prooplomeianocortin mRNA levels in the anterior lobe of the pituitary were not significantly altered after acute cocaine injections on day 1 or day 2. On day 14 of chronic binge-pattern cocaine administration, decreased hypothalamic CRF mRNA levels and an attenuated elevation in plasma corticosterone levels were found. After 10 days of withdrawal from 14-day binge cocaine, CRF mRNA returned to basal levels. CRF mRNA levels in the amygdala were also significantly increased on day 1 and returned to basal values on day 2. Chronic (14-day) binge cocaine administration did not alter CRF mRNA levels in the amygdala. These results suggest that the attenuated response in the hypothalamic-pituitary-adrenal axis to chronic binge cocaine administration is coupled to the cocaine-induced decreases in CRF gene expression in the hypothalamus and that activation of CRF gene expression in extrahypothalamic regions may have implications for a molecular understanding of the behavioral responses to cocaine.

Adrenocorticotropic Hormone↗
PubMed1999

Immunohistochemical localization of corticotropin-releasing factor in the brain and corticotropin-releasing factor and thyrotropin-stimulating hormone in the pituitary of chinook salmon (Oncorhynchus tshawytscha).

This report describes the distribution of corticotropin-releasing factor (CRF)-like immunoreactivity in the brain and the contiguous localization of CRF- and thyrotropin-stimulating hormone (TSH)-like immunoreactivity in the pituitary of hatchery-reared, juvenile chinook salmon (Oncorhynchus tshawytscha). Results show that CRF-immunoreactive cell bodies exist in the parvocellular and magnocellular nuclei of the preoptic area and in a ventral hypothalamic region corresponding to the nucleus lateralis tuberis. CRF-immunoreactive fibers are observed along the rostral edge of the hypothalamus, in the pituitary stalk, and in the pituitary gland. Within the pituitary, CRF-immunoreactive fibers, with terminal-like boutons, were distinguishable in the neurohypophysis, pars distalis (PD), and pars intermedia (PI). In the PD, the CRF-immunoreactive fibers terminate in regions that contain TSH-positive pituitary cells. From this study, we conclude that CRF-immunoreactive fibers travel through, and terminate in, the neurohypophysis. CRF-immunoreactive fibers were also observed to terminate within the basement membrane and within the PD and PI of the adenohypophysis. Furthermore, the contiguous localization of CRF-immunoreactive fibers and TSH-immunoreactive pituitary cells suggests that CRF may mediate release of TSH.

Animals↗
PubMed1993

Metyrapone induced increase in plasma corticotropin is not associated with changes in peripheral venous arginine vasopressin or corticotropin releasing factor.

The responses of the "stress hormones" cortisol, 11-deoxycortisol, ACTH, vasopressin (AVP), and corticotropin releasing factor (CRF) were studied in 6 normal males in response to acute cortisol deficiency induced by the 11-beta-hydroxylase inhibitor, metyrapone. A 750 mg dose was administered orally at 08:00 h on day 1 and at 4 hourly intervals over a 24-h period. A 20 mg tablet of hydrocortisone or placebo was then given at 08:00 h on day 2, according to a randomized cross-over design. Each subject was restudied after an interval of at least one month. Blood samples were taken for all hormones at 08:00 h on day 1 and at 04:00 h on day 2. Thereafter ACTH and AVP were sampled at 10-min intervals, CRF at 20-min intervals, and cortisol and 11-deoxycortisol at hourly intervals until 12:00 h on day 2. Cortisol (mean +/- SE) fell from 628 +/- 218 nmol/l at 08:00 h (day 1) to a minimum of 230 +/- 78 nmol/l at 05:00 h on day 2. Plasma 11-deoxycortisol rose from 14.0 +/- 0.8 nmol/l to a maximum of 622 +/- 36 nmol/l and plasma ACTH rose from 8.71 +/- 1.64 pmol/l to a maximum of 166.2 +/- 57.5 pmol/l. Diurnal rhythmicity of plasma ACTH was maintained. There was no detectable change in plasma levels of AVP or CRF from baseline (AVP 2.5 +/- 0.8 pmol/l, CRF 3.4 +/- 0.5 pmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

Pituitary and hypothalamic hormones in normal and neoplastic adrenal medullae: biologically active corticotropin-releasing hormone and corticotropin.

Six normal and 8 neoplastic adrenal medullae were assayed for several immunoreactive (IR) proopiomelanocortin (POMC) and hypothalamic peptides. IR-POMC peptides were found in normal and tumor tissue in concentrations ranging from 0.0003 to 0.1% of those in pituitary. Their molecular sizes resembled those of pituitary intermediate lobe POMC peptides. No intact POMC was found. One pheochromocytoma contained fully bioactive IR-adrenocorticotropic hormone (IR-ACTH; Mr approximately 4,500) and an intermediate-sized (Mr approximately 10,000) IR-ACTH with approximately 69% bioactivity. Normal and tumorous medullae contained IR-corticotropin-releasing hormone (CRH) in concentrations ranging from 0.6 to 4% of those in hypothalamus except for one pheochromocytoma that contained 40 times that amount of IR-CRH, which was chromatographically indistinguishable from hypothalamic CRH and fully bioactive. IR-somatostatin and IR-growth hormone-releasing hormone were found in both tissue types, but IR-gonadotropin-releasing hormone and IR-thyrotropin-releasing hormone (TRH) were not, although IR-histidyl-proline diketopiperazine, a putative TRH metabolite, was found. IR-arginine vasopressin was found in two normal medullae, but not in pheochromocytomas.

Adrenal Gland Neoplasms↗