Photosynthesis of vitamin D3 in cats.
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Animals↗
Biomedical subjects
J A Mol
Publications and source records attributed to J A Mol.
Production of antibodies to biosynthetic human growth hormone in the dog.
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Animals↗
Dietary vitamin D dependence of cat and dog due to inadequate cutaneous synthesis of vitamin D.
As in herbivores and omnivores, the biosynthesis of vitamin D3 in the skin exposed to ultraviolet (uv) light is generally expected to also occur in the dog and the cat. The purpose of this in vitro study was to measure the concentrations of vitamin D3 and its precursor 7-dehydrocholesterol (7DHC) in dog and cat skin before and after a quantitatively and qualitatively standardized exposure to uv light. The results are compared to those obtained by the same method in the skin of the rat. The efficiency of extracting 7DHC and vitamin D3 from skin was 72 +/- 8% and 67 +/- 3%, respectively. In dog and cat skin the concentrations of nonesterified 7DHC were below the detection limit of the HPLC system. Therefore, skin extracts were saponified and total 7DHC and vitamin D3 concentrations were measured by normal-phase HPLC. Before irradiation with uv-B light the total concentrations of 7DHC were 1858 +/- 183, 1958 +/- 204, and 17,620 +/- 2345 ng/cm2 skin (mean +/- SEM; n = 5) for the dog, the cat, and the rat, respectively. The corresponding concentrations of vitamin D3 were 211 +/- 44, 193 +/- 18, and 161 +/- 32 ng/cm2 skin for the dog, the cat, and the rat, respectively. Irradiation of standard solutions of 7DHC with 0.15 J uv-B light/min resulted in a time-dependent decrease in 7DHC and a concomitant increase in previtamin D3.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Predicted primary and antigenic structure of canine corticotropin releasing hormone.
Although the dog has been recognized as a useful model for the study of the cerebrospinal and peripheral actions of corticotropin releasing hormone (CRH) the exact amino acid composition of canine CRH is still unknown. In the present study the structure of canine CRH was predicted from the partial sequence of the gene encoding canine CRH. The CRH gene was amplified from genomic DNA obtained from white blood cells by a polymerase chain reaction and subsequently sequenced using the dideoxy method. The likely structure of canine CRH is: SEEPPISLDLTFHLLREVLEMARAEQLAQQAHSNRKLMEII-NH2, which is identical to the structure of human, rat and equine CRH. PEPSCAN analysis of 3 different CRH antisera predicted an antiserum raised against a conjugate of human CRH and CNBr -activated thyroglobulin to be the antiserum of choice for the measurement of CRH in the dog. Preliminary data confirmed the existence of the highest cross-reactivity of a canine hypothalamus extract, known to have a high content of CRH, with antisera directed against human, rat CRH. As a result of the present study immunological tools for CRH estimations are characterized. Also, a homologous DNA probe for in situ hybridizations has become available for further investigations.
Amino Acid Sequence↗
Progestin-induced growth hormone excess in the dog originates in the mammary gland.
In the dog endogenous progesterone and synthetic progestins may incite overproduction of GH, resulting in acromegaly and insulin resistance. This progrestin-induced excessive GH secretion is characterized by disappearance of the pulsatile secretion pattern and insensitivity to both stimulation with GHRH and inhibition with a somatostatin analog. This progestin-induced GH hypersecretion is not associated with neoplastic transformation at the pituitary level. These observations were the impetus for a search of a possible extrapituitary site of GH production. In four ovariohysterectomized dogs elevated plasma GH levels (46.5 +/- 7.7 micrograms/liter; mean +/- SEM) were induced by administration of synthetic progestins. In these dogs hypophysectomy did not led to a significant decrease in plasma GH levels. Analysis of the GH content of various tissue homogenates revealed that the highest GH immunoreactivity was found in extracts of the mammary gland. Ectopic production of GH in the mammary gland was confirmed by lowering of plasma GH concentration to values within the reference range within 2 h after complete mammectomy in two dogs with progestin-induced elevations of plasma GH levels. In one of these dogs the arterial and elevations of plasma GH levels. In one of these dogs the arterial and venous GH concentrations across the mammary gland were measured and an arterio-venous GH gradient was demonstrated. Displacement studies in the RIA and analysis by reversed-phase HPLC revealed that mammary-derived GH is highly similar to pituitary-derived GH. Immuno-histochemical staining revealed that GH immunoreactivity was localized in focal areas of hyperplastic ductular epithelium. In mammary tissue of healthy untreated female dogs no GH immunoreactivity was found. It is concluded that treatment of dogs with synthetic progestins can induce the overproduction of GH in the mammary gland. This GH is biologically active, highly similar to pituitary derived GH, and originates from foci of hyperplastic ductular epithelium of the mammary gland.
Animals↗
Effect of pericardiocentesis on circulating concentrations of atrial natriuretic hormone and arginine vasopressin in dogs with spontaneous pericardial effusion.
Factors regulating the secretion of atrial natriuretic hormone (ANH) and arginine vasopressin (AVP) have not been elucidated fully. In several studies the release of these peptides has been studied by inducing both increased atrial pressure and atrial distension. A few studies employ cardiac tamponade, allowing the effect of atrial pressure and atrial stretch to be studied separately. In eleven dogs with spontaneous cardiac tamponade the effect of pericardiocentesis on circulating concentrations of ANP and AVP was studied. Pericardiocentesis was followed by a prompt rise in (non-elevated) plasma ANH concentrations from 21.6 +/- 7.3 to 65.4 +/- 17.1 pmol/l (mean +/- SEM). The initially slightly elevated AVP concentration of 5.5 +/- 1.5 pmol/l declined following pericardiocentesis to 2.1 +/- 0.5 pmol/l. In three dogs the systolic arterial pressure was measured indirectly and the central venous pressure was measured with a fluid-filled catheter. Before and after pericardiocentesis arterial pressure readings did not change significantly. Central venous pressure values showed an immediate very steep significant decrease after centesis. It is concluded that ANH release is primarily regulated by stretch and not by atrial pressure, that plasma AVP concentrations are moderately elevated in cardiac tamponade and that in cardiac tamponade pericardiocentesis causes a rapid decline in plasma AVP concentration.
Animals↗
Responsiveness to corticotropin-releasing hormone and vasopressin in canine Cushing's syndrome.
Corticotropin-releasing hormone (CRH) and vasopressin are the most important hypothalamic factors regulating adrenocorticotropic hormone (ACTH) secretion. In this study we have investigated the responsiveness of the pituitary-adrenocortical axis to intravenous administration of CRH or lysine vasopressin (LVP) in 16 control dogs, 22 dogs with pituitary-dependent hyperadrenocorticism and five dogs with hyperadrenocorticism due to an adrenocortical tumor, using doses of CRH and LVP that caused equivalent ACTH responses in the control dogs. After CRH administration, the increment in plasma ACTH was significantly (p < 0.05) lower in dogs with pituitary-dependent hyperadrenocorticism (221 +/- 53 ng/l) than that in control dogs (279 +/- 41 ng/l). In the dogs with pituitary-dependent hyperadrenocorticism, the relative increases in ACTH after CRH were significantly (p < 0.05) lower than those after LVP. Despite the absence of an increase in ACTH following LVP administration in dogs with hyperadrenocorticism due to an adrenocortical tumor, there was a significant increase in plasma cortisol, the increment (790 +/- 238 nmol/l) being not statistically different from that in the control dogs (412 +/- 37 nmol/l). We conclude that in spite of the changes inherent to pituitary-dependent hyperadrenocorticism, i.e. neoplastic transformation of corticotropic cells and hypercortisolism, there is persistence of responsiveness to hypophysiotropic hormones. The ACTH secretion by corticotropic cells in pituitary-dependent hyperadrenocorticism was relatively less sensitive to stimulation with CRH than with LVP. Adrenocortical tumors develop an aberrant sensitivity to LVP.
Adrenal Cortex Neoplasms↗
Progestin treatment in the dog. I. Effects on growth hormone, insulin-like growth factor I and glucose homeostasis.
The effects of two synthetic progestins, medroxyprogesterone acetate (MPA) and proligestone (PROL), on the release of growth hormone (GH) and glucose metabolism were studied in two groups of eight ovariohysterectomized dogs. Eight injections of long-acting progestins were administered at 3-week intervals. Recovery was studied in four dogs of each treatment group in the 6 months following cessation of progestin administration. Treatment with both MPA and PROL resulted in similar increases in plasma levels of GH and insulin-like growth factor I (IGF-I). The GH responses to both clonidine and growth hormone-releasing hormone became impaired. In neither treatment group did the elevated plasma GH levels decrease after administration of the synthetic somatostatin analogue SMS 201-995. The size and shape of the pituitary gland were not changed by progestin treatment. After cessation of progestin administration, basal plasma levels of GH and IGF-I did not return to pretreatment values. The GH response to growth hormone-releasing hormone remained impaired for at least 6 months after the last progestin administration. In both treatment groups, glucose homeostasis was sustained initially by increased insulin production. Prolonged treatment with MPA and PROL resulted in glucose intolerance. No amelioration was observed during the recovery period in either group. A small number of dogs developed diabetes mellitus. In more than 50% of the dogs in both treatment groups small mammary tumours developed. The recently discovered local production of GH probably played a role in mammary tumorigenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Cortex↗
Progestin treatment in the dog. II. Effects on the hypothalamic-pituitary-adrenocortical axis.
The effects of two synthetic progestins, medroxyprogesterone acetate (MPA) and proligestone (PROL), on the hypothalamic-pituitary-adrenocortical (HPA) axis were studied in two groups of eight ovariohysterectomized dogs each. Eight injections of long-acting progestins were administered at 3-week intervals. Recovery of the HPA axis was studied in four dogs of each group in the following 6 months. Basal levels of adrenocorticotrophin (ACTH) and cortisol in plasma and the urinary corticoid/creatinine ratio were measured. The responsiveness of the HPA axis was investigated by stimulation with ovine corticotrophin-releasing hormone. Both MPA and PROL caused sawtooth patterns of suppression of basal ACTH and cortisol levels in plasma, synchronous with the time of administration. The suppression of the adrenocortical component of the HPA axis was most pronounced. Adrenocorticotrophin production also was affected but to a lesser extent and occurred especially in PROL-treated dogs. Soon after the cessation of progestin administration ACTH levels increased, sometimes with a rebound. In both groups basal cortisol levels and urinary corticoid/creatinine ratios did not return to pretreatment levels until 6 months after the last progestin injection. It is concluded that MPA and PROL act as glucocorticoid agonists and suppress the HPA axis. The suppression at the adrenocortical level may last for 6 months.
Adrenal Cortex Hormones↗
Growth and growth hormone in the dog.
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Animals↗
Comparison of in vivo and in vitro corticotropin-releasing hormone-stimulated release of proopiomelanocortin-derived peptides in cats.
In 6 cats, the effect of IV administration of various concentrations of ovine corticotropin-releasing hormone (oCRH) on plasma concentrations of cortisol, alpha-melanocyte-stimulating hormone (alpha-MSH), and adrenocorticotropic hormone (ACTH) was measured. After administration of 1.0 microgram of oCRH/kg of body weight, significant (P < 0.05) increases in plasma cortisol, alpha-MSH, and ACTH concentrations were observed. After administration of 0.1 microgram of oCRH/kg, significant increases were found only for cortisol and ACTH concentrations. In vitro release of ACTH from dispersed feline pars distalis cells in primary culture stimulated by oCRH and arginine vasopressin (AVP) was dose-dependent. Maximal stimulation was achieved by 1 nM oCRH or 100 nM AVP. The oCRH-stimulated ACTH release was partially inhibited by dexamethasone, and AVP-induced release was completely inhibited. Pars intermedia cells released 20 times as much alpha-MSH as ACTH. A dose-dependent inhibition of alpha-MSH release was induced by the dopamine agonist, bromocriptine. This inhibition could be partially abolished by coincubation with haloperidol. Bromocriptine had no effect on release of ACTH. In conclusion, oCRH stimulates the pars distalis and pars intermedia of the pituitary gland of cats. Release of ACTH is stimulated by a direct effect on the pars distalis. In addition, in cats, oCRH is a more potent secretagogue than is AVP. The MSH release from the pars intermedia is sensitive to dopaminergic inhibition, indicating that dopamine may have a central role in regulation of MSH secretion in cats.
Adrenocorticotropic Hormone↗
Disturbed release of growth hormone in mature dogs: a comparison with congenital growth hormone deficiency.
An acquired defect in growth hormone secretion in mature dogs has been associated with some forms of generalised alopecia. In an attempt to elucidate the pathogenesis of the disturbance in growth hormone release, the plasma concentrations of growth hormone and insulin-like growth factor I (IGF-I) were measured in two seven-year-old poodles with alopecia and, for comparison, in two young German sheperd dogs with congenital hyposomatotropism (pituitary dwarfism). In the poodles the basal concentrations of growth hormone were low, although often above the detection limit of the assay. The concentrations of IGF-I were in the reference range for healthy poodles. No growth hormone could be detected in the plasma of the German sheperd dogs and the concentrations of IGF-I were very low. Stimulation with clonidine and growth hormone releasing hormone (GHRH) before and after repeated injections of GHRH did not result in significant increases in growth hormone concentrations in plasma. The concentrations of growth hormone in the poodles fluctuated at low levels during the test period. In the German sheperd dogs the levels of growth hormone remained unmeasurable during the stimulation tests. It was concluded that in the two poodles the basal concentrations of growth hormone were sufficient to maintain normal IGF-I concentrations, and thus the release of growth hormone was considered appropriate. Based upon measurements of urinary corticoids and a review of the literature it is suggested that the lack of a growth hormone response to stimulation was due to the enhanced release of somatostatin as a result of mild and fluctuating hyperadrenocorticism.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Cortex Hormones↗
Age-related plasma concentrations of growth hormone (GH) and insulin-like growth factor I(IGF-I) in Great Dane pups fed different dietary levels of protein.
During a 20-week study, 17 Great Dane dogs, 7 weeks of age, were used to study the influence of 3 isoenergetic diets differing in dietary protein levels (i.e., 31.6%, 23.1%, and 14.6% on a dry matter basis) on body weight, growth in length, and age-related plasma GH and IGF levels. Significant differences occurred in weekly body weight gain of the high- and low- protein groups only in the fourth week of the study. There was a significant decrease in mean basal plasma GH values with time from 14.8 +/- 2.2, 13.7 +/- 2.2, and 14.3 +/- 2.2 micrograms/l in the second week to 2.3 +/- 1, 0.7 +/- 0.4, and 1.8 +/- 0.7 microgram/l in the last week of the study for the high-, normal- and low-protein groups, respectively. Differences among groups were not significant. There was a positive correlation between the decrease in weekly body weight gain and plasma GH concentration in all 3 groups. IGF-I concentrations in plasma did not change consistently with age and were not correlated with plasma GH values. Significant differences in plasma IGF-I concentrations were found between groups at 15 weeks of age. Preliminary results of measurements of IGF receptors in the membranes of growth plate cartilage of long bones of 5 dogs revealed that homologous displacement of 125I-labeled IGF-I binding resulted in similar curves. A single binding site for IGF-I was assumed. The large number of type II IGF receptors in 7 dogs suggests a key role for IGF-II in postnatal skeletal growth. The results of this study demonstrate for the first time that in Great Dane pups basal GH concentrations in plasma decrease between 7 and 27 weeks of age, parallel to the decrease in growth velocity, whereas the plasma IGF-I concentrations remain relatively high and unchanged. The slight but statistically significant effects of low-protein feeding on growth velocity and circulating concentrations of IGF-I indicate that a diet containing 14.6% protein on a dry matter basis (13% protein as metabolizable energy) is marginal for growing Great Dane pups between 7 and 17 weeks of age.
Aging↗
Increased neuroendocrine reactivity and decreased brain mineralocorticoid receptor-binding capacity in aged dogs.
The effects of aging on the regulation of the hypothalamus-pituitary-adrenocortical (HPA) system of the dog were investigated. For this purpose, we compared 11 healthy dogs, 11-14 yr old, with 14 young mature dogs, 18-24 months of age. Significantly higher basal HPA activity in the old dogs was indicated by their higher resting plasma concentrations of ACTH, alpha MSH, and cortisol over a 6-week period and higher cortisol excretion in 24-h urine. After stress by immobilization as well as by light electric foot shocks and after i.v. administration of 1 microgram/kg CRH, the old dogs had higher peak levels of ACTH and cortisol, but not of alpha MSH. The areas under the curve, corrected for the basal levels, for ACTH and cortisol after these challenges were also greater in the old dogs. The half-times to reach a 50% increment and a 50% decrement in the time-concentration curves of ACTH and cortisol were similar in old and young dogs. There were no differences between the old and young dogs in their response to i.v. administration of 0.01 mg/kg dexamethasone. The clearance of [14C]cortisol from plasma, as calculated in a two-compartment model, was significantly reduced in aged dogs. In the old dogs, the stress- and CRH-induced cortisol peaks were relatively higher than those of ACTH, and their adrenals weighed significantly more, suggesting chronic hyperadrenocorticotropism. Aging had a markedly different effect on the two types of corticosteroid receptors in brain and pituitary. The binding capacity of type II or glucocorticoid receptors (GRs) in the old dogs was unchanged compared with that in the young dogs in all investigated brain structures except the anterior pituitary, in which the number of GRs was increased up to 170%. Type I or mineralocorticoid receptor (MR)-binding capacity was largely decreased in the brain of old dogs. The MR levels in old dogs, expressed as a percentage of the corresponding levels in young dogs, were 34% in the dorsal hippocampus, 58% in the ventral hippocampus, 37% in the septum, and 54% in the hypothalamus. In the anterior pituitary, MR capacity was unchanged. There was no difference between Kd values of MR and GR binding in young and old dogs. We conclude that these aged dogs had elevated basal HPA activity, characterized by increased levels of basal ACTH and cortisol in plasma and of urinary cortisol excretion and by hyperreactivity of ACTH and cortisol secretion in response to challenge by stress or CRH.(ABSTRACT TRUNCATED AT 400 WORDS)
Adrenal Cortex↗
Changes in plasma cortisol, corticotropin, and alpha-melanocyte-stimulating hormone concentrations in cats before and after physical restraint and intradermal testing.
In 6 cats, mean +/- SEM baseline plasma concentrations of cortisol, corticotropin, and alpha-melanocyte-stimulating hormone (alpha-MSH) were 87 +/- 16 nmol/L, 73 +/- 14 ng/L, and 129 +/- 12 ng/L, respectively. The cats were subjected to: handling and subsequent skin testing without anesthesia; anesthesia with 50 mg of ketamine HCl and 2.5 mg of diazepam given IV, immediately followed by handling and skin testing; and anesthesia and handling as previously described, but without skin testing. Significant (P < 0.05; multivariate analysis for repeated measures) increase in plasma cortisol, corticotropin, and alpha-MSH concentrations was observed until 20 minutes after the start of the experiments in cats undergoing physical restraint and subsequent skin testing with or without preceding anesthesia. These responses were largely abolished when anesthesia with ketamine and diazepam was only followed by handling. We conclude that, during stress in cats (in contrast to dogs), the pituitary intermediate lobe is activated to secrete alpha-MSH. In addition, the cortisol response after skin testing of cats under anesthesia may be a reasonable explanation for the reported weak skin test reactivity in cats.
Adrenocorticotropic Hormone↗
Canine growth hormone regulation: new insights.
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Animals↗
Corticoid production by four dogs with hyperfunctioning adrenocortical tumours during treatment with mitotane (o,p'-DDD).
In two dogs with hyperadrenocorticism due to an adrenocortical tumour, treatment with o,p'-DDD was started. Their hormonal response was monitored by measurements of the urinary corticoid/creatinine ratio. In one dog, two courses of 10 days treatment with o,p'-DDD were ineffective, whereas in the other dog the urinary corticoids decreased to very low levels after only six days of treatment, and corticosteroid supplementation had to be started. Two other dogs received o,p'-DDD according to a protocol used for the treatment of pituitary-dependent hyperadrenocorticism which aims at the complete destruction of the adrenal cortices, with substitution for the induced hyperadrenocorticism. Both dogs made a good recovery and their urinary corticoid/creatinine ratio decreased to within the reference range. In one of them the tumour had decreased considerably in size by five weeks after the start of the treatment.
Adenoma↗
In vivo studies on the effects of ovine corticotrophin-releasing hormone, arginine vasotocin, arginine vasopressin, and haloperidol on adrenocortical function in the racing pigeon (Columba livia domestica).
This study investigates the effects of in vivo administration of pituitary stimulants in racing pigeons (Columba livia domestica). Plasma corticosterone concentrations were measured following intravenous administration of ovine corticotrophin-releasing hormone (oCRH) (0.1, 1, 10, and 100 micrograms/kg), arginine vasopressin (AVP) (0.01, 0.1, 1, and 10 micrograms/kg), arginine vasotocin (AVT) (0.01, 0.1, 1, and 5 micrograms/kg), and haloperidol (0.05, 0.5, and 5 micrograms/kg). Compared with mammals the pituitary-adrenocortical system of the pigeon appeared to be less sensitive to stimulation with oCRH, although high doses were well tolerated and gave a clear response. Both AVP and AVT stimulated corticosterone secretion, AVT in a more pronounced dose-dependent manner than AVP. The natural neurohypophysial peptide in birds, AVT, was less well tolerated in high doses than AVP. The clear response to haloperidol indicates that the hypothalamo-pituitary-adrenocortical system is under dopaminergic inhibition. Of the pituitary stimulants tested AVP (10 micrograms/kg) and oCRH (100 micrograms/kg) are the most appropriate for testing the integrity of the pituitary-adrenocortical system in the pigeon.
Adrenal Cortex↗