Biomedical subjects

R J Kemppainen

Publications and source records attributed to R J Kemppainen.

At least 37 records · Page 2Linked to original sources

PubMed1995

Effects of short-term cortisol infusion on growth hormone-releasing hormone stimulation of growth hormone release in sheep.

Excess production or long-term administration of glucocorticoids is detrimental to longitudinal growth in people and rats. A portion of this effect is attributed to cortisol inhibition of growth hormone (GH). Glucocorticoid effects are usually studied in subjects under long-term treatment with synthetic, more potent glucocorticoids, and, to the authors' knowledge, have not been examined in domestic animals. We sought to examine the effects of cortisol infusion on GH release in sheep. Cortisol infusion into castrated, male Suffolk sheep (1 to 1.5 years old) caused a significant (P < 0.0001) increase in cortisol concentration. Basal GH release was not affected over the 4-hour period of infusion. Growth hormone-releasing hormone administration stimulated GH release in both groups (P < 0.001); however, the control group had a greater response to growth hormone-releasing hormone than did the cortisol infused group (P < 0.0001). These results were duplicated in cultured sheep pituitary cells. Cortisol inhibition of GH release may be mediated via enhanced somatostatin release, owing to a direct inhibition of somatotrope function, or a combination of both mechanisms. Because of effects of stress and disease in increasing cortisol concentration, additional study of the mechanisms for cortisol inhibition of GH release in sheep needs to be performed.

Analysis of Variance↗

PubMed1995

Prolonged gestation, decreased triiodothyronine concentration, and thyroid gland histomorphologic features in newborn foals of mares grazing Acremonion coenophialum-infected fescue.

Newborn foals of mares grazing on Acremonium coenophialum-infected fescue pasture throughout gestation or from gestation day 300 to parturition had increased gestation duration and decreased serum triiodothyronine concentration. Pregnant mares were allotted to 4 treatments: grazing continuously on endophyte-free (E-) fescue, grazing continuously on endophyte-infected (E+) fescue, grazing on E+ fescue from gestation day 300 to parturition, and grazing on E+ fescue from conception to gestation day 300. Morphometric studies indicated that foals born to mares exposed to endophyte late in gestation had large, distended thyroid follicles lined by flat cuboidal epithelial cells. Mean triiodothyronine concentration in foals exposed to endophyte (395.2 ng/dl) was decreased (P < 0.01), compared with mean values in control foals (778.0 ng/dl). Thyroxine and reverse triiodothyronine concentrations were not significantly different among groups. Foal organ weight as a percentage of foal body weight was not significantly different among experimental groups.

Acremonium↗

PubMed1994

Preservative effect of aprotinin on canine plasma immunoreactive adrenocorticotropin concentrations.

The susceptibility of adrenocorticotropin (ACTH) in canine blood and plasma to enzymatic degradation has limited the availability of endogenous ACTH assay for veterinary use. This study examined if a proteinase (enzyme) inhibitor, aprotinin, mixed with blood at the time of collection, would limit the loss of immunoreactive (IR) ACTH from canine plasma stored at various temperatures. Blood was collected from laboratory-maintained dogs or dogs with hyperadrenocorticism and placed into EDTA-containing tubes in the presence or absence of aprotinin. Plasma obtained was stored for 4 d at temperatures ranging from -86 degrees C to room temperature (22 degrees C). Results showed that addition of aprotinin preserved IR-ACTH concentrations in plasma stored for 4 d at temperatures < or = 4 degrees C, or in unfrozen plasma stored inside insulated shipping containers containing frozen refrigerant packs. Plasma collected with aprotinin and stored at 22 degrees C showed a slight (17-23%) but significant (P < 0.05) decline in IR-ACTH. Unfrozen plasma collected without aprotinin showed significant (P < 0.05) loss of IR-ACTH during storage under identical conditions. These data indicate that aprotinin has a profound preservative effect upon canine plasma IR-ACTH and that it may be possible to submit unfrozen samples collected with this inhibitor to appropriate reference laboratories for analysis of IR-ACTH.

Adrenocorticotropic Hormone↗

PubMed1994

Etiopathogenesis of canine hypothyroidism.

Hypothyroidism in dogs usually results from a progressive destruction of the thyroid, associated with either lymphocytic thyroiditis or idiopathic atrophy. Both syndromes seem to occur with approximately equal frequency. Lymphocytic thyroiditis, which resembles Hashimoto's thyroiditis in humans, is probably an autoimmune disease, and patients often show thyroid autoantibody titers in circulation. By contrast, the pathogenesis of idiopathic atrophy is unclear, and the thyroid seems simply replaced by adipose and connective tissue.

Animals↗

PubMed1994

Glucocorticoid negative feedback in sheep corticotrophs: a comparison with AtT-20 corticotroph tumor cells.

Early glucocorticoid feedback in sheep anterior pituitary (AP) cells was compared and contrasted with that in mouse pituitary tumor AtT-20 cells. Dexamethasone (DEX) inhibited corticotropin-releasing hormone (CRH)-stimulated adrenocorticotropin (ACTH) release in a concentration- and time-dependent manner with similar potency amongst cell types. This inhibition was mediated through type II glucocorticoid receptors and required the synthesis of new protein. However, stimulation of protein kinase C with phorbol 12-myristate 13-acetate (PMA) resulted in greater ACTH release and greater inhibition by DEX in sheep AP cells. In contrast to sheep AP cells, AtT-20 cells were insensitive to glucocorticoids when secretion was stimulated by KCl depolarization or the voltage-dependent calcium channel agonist, maitotoxin (MTX). In both cell types, CRH-, KCl-, and MTX-stimulated ACTH release was inhibited by the calcium channel blocker, nifedipine (NIF). Whereas NIF also inhibited PMA-induced ACTH secretion in AtT-20 cells, it did not in sheep AP cells. These data demonstrate that early glucocorticoid feedback is operative in sheep corticotrophs and that AtT-20 cells appear to serve as an appropriate mechanistic model for aspects of negative feedback when the CRH-protein kinase A pathway is activated but may not be appropriate when ACTH secretion is activated via other intracellular signaling pathways.

Adrenocorticotropic Hormone↗

PubMed1994

Glucocorticoids do not affect intracellular calcium transients in corticotrophs: evidence supporting an effect distal to calcium influx.

The influx of extracellular calcium is a critical step involved in the stimulated release of adrenocorticotropin (ACTH) from pituitary corticotrophs. It has been proposed that the mechanism of early glucocorticoid feedback is mediated through inhibition of stimulus-evoked calcium transients. We tested this hypothesis using corticotrophic mouse pituitary AtT-20 cells by coevaluating secretory dynamics and cytosolic calcium transients. In static monolayer culture and in a dynamic microperifusion system, dexamethasone (DEX, 100 nM, 2 h) significantly inhibited ACTH secretion stimulated by corticotropin-releasing hormone (CRH, 100 nM). When ACTH was stimulated by KCl (56 mM) depolarization or the voltage-dependent calcium channel agonist, maitotoxin (MTX, 1 ng/ml), DEX did not inhibit secretion. In contrast, CRH-, KCl-, and MTX-stimulated ACTH secretion were significantly inhibited in static monolayer culture when cells were pretreated with the voltage-dependent calcium channel blocker, nifedipine (NIF, 1 microM, 15 min), confirming the requirement for the influx of extracellular calcium. Intracellular calcium was measured under similar culture conditions in populations of cells grown on coverslips, utilizing the fluorescent calcium indicator, fura-2. DEX had no effect on basal, spike, or plateau calcium levels in response to CRH, KCl or MTX stimulation. For example, CRH stimulation resulted in an increase in intracellular calcium from a basal concentration of 90 +/- 3.1 nM (mean +/- SE) to a plateau of 222 +/- 8.7 nM, whereas the plateau after DEX was 225 +/- 4.1 nM. In contrast, NIF significantly lowered the stimulated calcium response to each secretagogue (spike and plateau). These results do not support the hypothesis that glucocorticoids suppress stimulated secretion of ACTH from corticotrophs through an effect on intracellular calcium transients. Instead, the data suggest that early glucocorticoid negative feedback occurs at a step(s) distal to the influx of extracellular calcium.

Adrenocorticotropic Hormone↗

PubMed1994

Cortisol inhibition of growth hormone-releasing hormone-stimulated growth hormone release from cultured sheep pituitary cells.

Cortisol inhibits growth hormone (GH) release in short-term culture and is stimulatory in long-term cultures of rat and human pituitary cells. This study sought to determine the in vitro effects of cortisol on GH release and the signal transduction pathways mediating the effects of cortisol on GH release from cultured ovine somatotrophs. Pituitary cells were dispersed with collagenase and placed in culture medium for 4 days. The data indicate that cortisol inhibited growth hormone-releasing hormone (GHRH)-stimulated GH release by at least 2 h. In short-term culture GHRH-, forskolin- and dibutyryl cyclic AMP-stimulated GH release were inhibited by cortisol, suggesting an effect distal to the membrane and involving a protein kinase A (PKA)-dependent pathway. GH release initiated by KCl was inhibited by cortisol, but GH release caused by the calcium ionophore A23187 was unaffected. This suggests a possible action of cortisol on the calcium channels. The inhibition by cortisol of the calcium-dependent secretion of GH release appeared to play a smaller role in mediating cortisol inhibition of GH release than that seen with PKA. Attempts to overcome cortisol inhibition of GH release using puromycin, arachidonic acid or pertussis toxin were unsuccessful. Since cortisol inhibition of GH release does not occur via the mechanisms found in other cell types, cortisol inhibition of pituitary cell secretions appears to be cell-specific rather than utilizing a single inhibitory mechanism. The majority of cortisol actions on the somatotroph appear to act at a site distal to the production of cyclic AMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Neurotransmitter receptor agonists regulate growth hormone gene expression in cultured ovine pituitary cells.

The regulation of growth hormone (GH) secretion and GH mRNA content by the dopaminergic agonist, bromocriptine (BRO); the beta-adrenergic agonist; isoproterenol (ISO); the alpha 1-adrenergic agonist, methoxamine (MET); the alpha 2-adrenergic agonist, clonidine (CLON); the serotonergic agonist, quipazine (QUIP); somatostatin (SS) and GH-releasing hormone (GHRH) were studied using cultured ovine anterior pituitary cells. Clonidine and BRO (10(-6) M) inhibited basal and GHRH (10(-10) M)-stimulated GH release. Bromocriptine enhanced GH mRNA content and potentiated the GHRH (10(-8) M)-stimulated content of GH mRNA, while CLON had no effect on GH mRNA. Quipazine had little effect on GH secretion and no effect on GH mRNA content. Methoxamine and ISO (10(-6) M) increased basal secretion of GH and both enhanced GHRH-stimulated GH secretion. Both MET and ISO increased GH mRNA content of cultured ovine pituitary cells. Somatostatin (10(-7) M) inhibited GHRH-stimulated GH secretion and GH mRNA accumulation. These results support the hypothesis that neurotransmitters may regulate or interact to further modulate pituitary hormone release. Moreover, the data indicate that neurotransmitters may not only regulate secretion but also regulate GH mRNA content and thus affect hormone synthesis.

Animals↗

PubMed1994

Molecular forms of beta-endorphin in the canine pituitary gland.

Acid extracts of anterior and intermediate lobes of the pituitary gland from 4 dogs were fractionated by cation-exchange high-performance liquid chromatography and analyzed by radioimmunoassay, using 2 antibodies: one specific for the midregion of beta-endorphin (beta-end) and the other specific for the N-terminal region of N-acetylated beta-END. Identification of peaks of canine beta-END immunoreactivity was based on the retention times relative to those of synthetic human beta-END standards, with predicted variations attributable to differences in the beta-END amino acid sequences between the 2 species. The canine anterior lobe was found to contain almost exclusively beta-END (1-31). By contrast, the intermediate lobe contained substantial amounts of N-acetylated and C-terminally shortened forms of beta-END. The predominant forms of beta-END in canine intermediate lobe were, in decreasing order of abundance: beta-END (1-27), beta-END (1-31), beta-END (1-26), Ac beta-END (1-27), Ac beta-END (1-26) and Ac beta-END (1-31). Individual beta-END immunoreactivity profiles varied, but the general pattern was consistent among the 4 dogs.

Amino Acid Sequence↗

PubMed1994

Adrenocorticotropic hormone and cortisol concentrations after corticotropin-releasing hormone stimulation testing in cats administered methylprednisolone.

The hypothalamic-pituitary-adrenocortical (HPA) axis was studied in 8 healthy cats after administration of supraphysiologic doses of methylprednisolone (MP). Ovine corticotropin-releasing hormone (oCRH) administration increased cortisol and adrenocorticotropic hormone (ACTH) concentrations. Significant (P < 0.05) suppression of cortisol and a trend toward suppression of ACTH was observed after 1 week of MP administration. The HPA axis quickly recovered from suppressive effects of MP 1 week after administration of the steroid was discontinued. Side effects of oCRH administration were minimal in 7 cats; however, 1 cat had a severe hypotensive reaction. Clinical abnormalities were not associated with MP administration. The HPA axis was suppressed by supraphysiologic doses of MP in all treated cats that lacked clinical signs consistent with iatrogenic HPA axis suppression. Despite the relatively active pars intermedia in cats, compared with human beings and dogs, feedback of MP on the HPA axis resulted in similar trends in oCRH-stimulated ACTH and cortisol concentrations as observed in human beings and dogs. Lack of consistent correlation between ACTH and cortisol concentrations was observed in 3 cats and possibly was related to the active pars intermedia in the cat.

Adrenocorticotropic Hormone↗

PubMed1994

Plasma concentrations of immunoreactive proopiomelanocortin peptides and cortisol in clinically normal cats.

We measured immunoreactive (IR) plasma concentrations of the proopiomelanocortin (POMC)-derived peptides (adrenocorticotropic hormone [ACTH]; beta-endorphin/beta-lipotropin [beta END/beta LPH]; and alpha-melanocyte stimulating hormone [alpha MSH]) and of cortisol in 100 clinically normal cats. Median plasma concentration of IR-ACTH was 2.7 pmol/L (range, < or = 1.1 to 22 pmol/L), of beta END/beta LPH was 28 pmol/L (range, 3.8 to 130 pmol/L), of alpha MSH was 36 pmol/L (range, < or = 3.6 to 200 pmol/L), and of cortisol was 35 nmol/L (range, 5 to 140 nmol/L). Plasma concentrations of IR-ACTH, alpha MSH, and beta END/beta LPH were at or below the assay sensitivity in 34, 3, and 0% of the cats, respectively. We did not detect a correlation between plasma concentrations of IR-ACTH and beta END/beta LPH (r = 0.23) or between plasma concentrations of IR-ACTH and alpha MSH (r = 0.19). However, there was a significant (P < 0.001) correlation between plasma concentrations of IR-beta END/beta LPH and alpha MSH (r = 0.81). There was not a significant correlation between plasma concentration of cortisol and plasma concentration of any of the IR-POMC peptides. High plasma concentrations of IR-alpha MSH and beta END, POMC peptides secreted predominantly by melanotrophs in other species, indicate that clinically normal cats have an actively secreting pars intermedia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1993

Hypothalamic peptide regulation of ACTH secretion from sheep pituitary.

The relative abilities of the hypothalamic peptides corticotropin-releasing factor (CRF), arginine vasopressin (AVP), oxytocin (OT), and angiotensin II (ANG II) to stimulate adrenocorticotropic hormone (ACTH) secretion from cultured sheep anterior pituitary cells were studied. Incubation of cells with CRF, AVP, and OT, but not ANG II, was associated with increased ACTH secretion. CRF and AVP were equally effective in stimulating ACTH release at 0.1 nM, but larger doses of each resulted in distinctly different ACTH secretory patterns. The minimally effective dose of OT was 10 nM; greater doses of this peptide resulted in ACTH secretory responses similar to those measured after addition of AVP. Cotreatment with ANG II did not affect the ACTH-secretory response to CRF, AVP, or OT. These data confirm that AVP is a potent stimulus for ACTH secretion from sheep anterior pituitary in vitro and also show that CRF is effective in low concentrations in releasing ACTH. In contrast, the data do not support a regulatory role for ANG II in stimulating ACTH release directly from sheep corticotroph cells.

Adrenocorticotropic Hormone↗

PubMed1993

Domperidone treatment enhances corticotropin-releasing hormone stimulated adrenocorticotropic hormone release from the dog pituitary.

While dopamine (DA) is known to inhibit pituitary intermediate lobe proopiomelanocortin (POMC) peptide secretion and synthesis in most species, its influence on anterior-lobe (AL) POMC peptide synthesis and secretion is less clear. We, therefore, sought to determine the effects of daily treatment with the DA receptor antagonist, domperidone (DOM), on secretion of the POMC peptides adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) from the dog pituitary, and on concentrations of another pituitary hormone regulated by DA, prolactin (PRL). Dogs treated for 7 days with DOM had significantly higher peak ACTH concentrations in response to corticotropin-releasing hormone (CRH) injection (329 +/- 37 pg/ml, mean +/- SD) than did controls (164 +/- 42 pg/ml). PRL was also significantly (p < 0.05) increased in samples collected on a daily basis after DOM injections (9.5 +/- 4.6 vs. 4.3 +/- 3.3 ng/ml in controls). However, plasma alpha-MSH concentrations were unaffected by DOM. In a subsequent study, dogs were again treated daily with DOM or vehicle (controls), and additionally were given dexamethasone (DEX) to block AL ACTH release. DEX-treated controls showed low daily and CRH-stimulated ACTH and cortisol concentrations (generally below assay sensitivity). In contrast, DEX + DOM-treated dogs had daily mean ACTH concentrations ranging from 10 +/- 8.1 to 32 +/- 26 pg/ml and mean peak post-CRH ACTH concentrations of 174 +/- 16 pg/ml. Although daily cortisol concentrations were below assay sensitivity, the mean peak post-CRH cortisol concentration was 6.7 +/- 1.8 micrograms/dl, indicating that the immunoreactive ACTH was biologically active.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1993

Effect of endotoxin on pituitary hormone secretion in sheep.

Endotoxin, a potent stimulator of the immune system and an important mediator in the pathophysiology of septic shock, has been shown to alter the release of certain hormones following its systemic administration. The purpose of this study was to determine the effects of endotoxin on pituitary hormone secretion both in vivo and in vitro in sheep, with emphasis placed on its effects on growth hormone (GH) release. Endotoxin (400 ng/kg i.v.) increased plasma GH, adrenocorticotropic hormone (ACTH), cortisol and prolactin, while it decreased luteinizing hormone (LH) pulse frequency (p < 0.05). Plasma levels of tumor necrosis factor, a major mediator of endotoxin effects, also increased following endotoxin administration. Endotoxin did not affect the GH response to human GH-releasing hormone. In vitro studies evaluated the effect of endotoxin to alter GH secretion from dispersed sheep anterior pituitary cells at dosages of 1, 10 and 50 micrograms/ml, with samples collected at 4, 8 and 24 h. Endotoxin increased pituitary GH secretion at 24 h for 1 microgram/ml (p < 0.05) and at all time periods for 10 and 50 micrograms/ml (p < 0.05). It also led to an increased release of ACTH and LH in vitro. The results of this study demonstrate the ability of endotoxin to alter pituitary hormone secretion both in vivo and in vitro in sheep, suggesting a direct effect of endotoxin on the pituitary gland.

Adrenocorticotropic Hormone↗

PubMed1993

Circulating concentration of dexamethasone in healthy dogs, dogs with hyperadrenocorticism, and dogs with nonadrenal illness during dexamethasone suppression testing.

Concentration of dexamethasone was determined in plasma or serum samples from dogs after i.v. administration of a low dose (0.01 mg/kg of body weight) or high dose (0.1 mg/kg) of dexamethasone. On the basis of history, clinical signs of disease, and degree of cortisol suppression in response to dexamethasone, dogs were assigned to these groups: healthy dogs, dogs with nonadrenal illness, and dogs with hyperadrenocorticism. Four hours after administration of the low dose of dexamethasone, concentration of the steroid was reduced (P < 0.05) in dogs with hyperadrenocorticism, compared with healthy dogs, but not compared with values from dogs with nonadrenal illness. By 8 hours after dexamethasone administration, values were similar across groups. Dexamethasone concentration 4 and 8 hours after high-dose administration was similar between healthy dogs and dogs with hyperadrenocorticism. Concentration of dexamethasone 4 and 8 hours after its administration overlapped after the 2 doses. For example, in 11 of 66 dogs from all groups, concentration measured 4 hours after the low dose was greater than the minimal concentration determined in the 18 dogs given the high dose. These data indicate that dexamethasone metabolism may be altered in dogs with hyperadrenocorticism, and that individuals may have appreciable variability in dexamethasone clearance. Such variability provides a possible explanation for false-positive and false-negative results associated with dexamethasone suppression testing in dogs.

Adrenocortical Hyperfunction↗

PubMed1993

Dose-response relation between plasma concentrations of corticotropin and cortisol after administration of incremental doses of cosyntropin for corticotropin stimulation testing in cats.

We compared the plasma cortisol and immunoreactive corticotropin (IR-ACTH) responses to incremental doses (1.25, 12.5 and 125 micrograms) of synthetic ACTH (cosyntropin) administered IV to 6 clinically normal cats. Mean plasma cortisol concentration increased significantly (P < 0.0001) after administration of all 3 doses of cosyntropin. After administration of the 1.25- and 12.5-microgram doses, plasma cortisol concentration peaked at 30 minutes, then decreased to values not significantly different from baseline concentration by 90 and 120 minutes, respectively. In contrast, after administration of the 125-micrograms dose, mean cortisol concentration peaked at 60 minutes and remained significantly (P < 0.05) higher than baseline values at 120 minutes. Compared with the 1.25- and 12.5-micrograms doses, administration of the 125-micrograms dose of cosyntropin induced significantly (P < 0.05) higher cortisol responses at 60, 90, and 120 minutes. Although individual cat's peak plasma cortisol concentration after administration of the 125-micrograms dose was higher than the peak value determined after administration of the 2 lower doses of cosyntropin, these differences were not statistically significant. Mean plasma IR-ACTH concentration increased significantly (P < 0.0001) and reached a maximal value at 30 minutes after administration of all 3 doses of cosyntropin. After administration of the 1.25- and 12.5-micrograms doses, plasma IR-ACTH concentration decreased to values not significantly different from baseline concentration by 60 and 120 minutes, respectively, whereas mean IR-ACTH concentration remained significantly (P < 0.05) higher than baseline values 120 minutes after administration of the 125-micrograms dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1992

Effects of steroids on the olfactory function of the dog.

Twenty-four (24) mature, mixed breed, healthy dogs weighing from 14.6 kg to 27.6 kg were used to study the effects of various steroids on the olfactory function of the dog using olfactory detection threshold as an index. Two odorants were used, viz; benzaldehyde and eugenol. Of the various steroids used, only dexamethasone produced classical signs of Cushing's syndrome in the dogs. However, all dogs that received either dexamethasone alone or hydrocortisone plus DOCA exhibited a significant elevation in the olfactory detection threshold for both odorants without any observable structural alteration of the olfactory tissue using light microscopy. On the other hand, neither DOCA, hydrocortisone alone, nor any of the vehicles used in the study significantly altered the olfactory function of the dogs. The results show that Cushing's syndrome can be experimentally produced in dogs using exogenous steroids and that this condition diminishes the olfactory capability of the dog without producing classical signs of the disease.

Adrenal Cortex Function Tests↗

PubMed1992

Effects of synthetic ovine corticotropin-releasing hormone on plasma concentrations of immunoreactive adrenocorticotropin, alpha-melanocyte-stimulating hormone, and cortisol in dogs with naturally acquired adrenocortical insufficiency.

We evaluated the effect of ovine corticotropin-releasing hormone (CRH) on plasma immunoreactive (IR) concentrations of ACTH, alpha-melanocyte-stimulating hormone, and cortisol in 8 dogs with naturally acquired adrenocortical insufficiency. Of the 7 dogs with primary adrenal insufficiency, 6 had markedly high basal plasma IR-ACTH concentrations and exaggerated ACTH responses to CRH administration, whereas 1 dog that was receiving replacement doses of prednisone at the time of testing had normal basal IR-ACTH concentrations and a nearly normal response to CRH. In contrast, the 1 dog with secondary adrenocortical insufficiency had undetectable basal plasma IR-ACTH concentrations, which failed to increase after administration of CRH. Basal plasma alpha-melanocyte-stimulating hormone concentrations in the dogs with adrenal insufficiency were within normal range and were unaffected by CRH administration. In all 8 dogs with adrenal insufficiency, plasma cortisol concentrations were low and did not increase after administration of CRH. Therefore, stimulation with CRH produced 2 patterns of plasma IR-ACTH response when administered to dogs with naturally acquired adrenal insufficiency. Dogs with primary adrenal insufficiency had high basal plasma IR-ACTH concentrations and exaggerated responses to CRH, whereas the dog with secondary adrenal insufficiency had undetectable basal plasma concentrations of IR-ACTH that did not increase after stimulation with CRH.

Adrenal Cortex Hormones↗