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C G Scanes

Publications and source records attributed to C G Scanes.

At least 163 records · Page 9Linked to original sources

Mechanism of renin release in exercising dog.

Exercise is associated with an increase in plasma renin activity (PRA). The purpose of this study was to determine the role of the prostaglandin (PG) and adrenergic pathways in the renin release with exercise in the dog. One group of animals (n = 4) was exercised under control untreated and indomethacin- and meclofenamate- (2 mg/kg) treated conditions. A 155% increase in PRA was not influenced by PG inhibition. In a second group (n = 7) PRA was 1.22 +/- 0.32, 3.29 +/- 1.59, 6.28 +/- 2.85, and 5.30 +/- 2.00 ng ANG I X ml-1 X h-1 at rest and during light, moderate, and heavy exercise, respectively. Guanethidine treatment (15 mg/kg) decreased mean PRA by 41, 50, 70, and 73% at rest and during the three levels of exercise, respectively. In a third group (n = 5) control exercise runs were repeated after metoprolol treatment. Selective beta 1-blockade completely abolished the increment in PRA observed with exercise. These data demonstrate that the elevation of PRA during exercise in the dog is mediated by increased sympathetic nerve activity involving beta 1-receptors and that it is not dependent on alterations in PG synthesis.

Animals↗

Comparative stimulation of growth hormone secretion in anaesthetized chickens by human pancreatic growth hormone-releasing factor (hpGRF) and thyrotrophin-releasing hormone (TRH).

Plasma concentrations of growth hormone (GH) were elevated in anaesthetized male domestic fowl following the intravenous administration of either synthetic human pancreatic GH-releasing factor 1-44 (NH2) (hpGRF) or synthetic thyrotrophin-releasing hormone (TRH). In 6-week-old chicks the plasma GH level was elevated between 5 and 10 min after the injection of hpGRF at doses between 1 and 80 micrograms/kg. The magnitude of the response increased with doses of hpGRF between 1 and 10 micrograms/kg but declined with higher doses. The GH concentration rapidly declined between 10 and 20 min and between 20 and 40 min after injection. The administration of TRH had similar effects on GH secretion, although the responses were greater than with comparable doses of hpGRF, and the most effective dose (1-1.4 micrograms/kg) was less than with hpGRF. In anaesthetized adult cockerels GH secretion was also increased by the administration of hpGRF (1-20 micrograms/kg) or TRH (0.1-80 micrograms/kg) and in both cases the dose-response relationship was biphasic. The maximal response to TRH in adult birds was again greater than that produced by hpGRF although the response was less than that elicited in immature birds and required a higher dose (20 micrograms/kg) of TRH. The optimal dose of hpGRF and the magnitude of the GH response induced in adult birds was comparable with that in immature chicks. These results demonstrate provocative effects of TRH and hpGRF on GH secretion in the domestic fowl. The sensitivity of the GH response to TRH suggests that it may have a physiological role in the hypothalamic control of GH secretion.

Age Factors↗

Self-suppression of corticosteroidogenesis: evidence for a role of adrenal 5 alpha-reductase.

Exogenous corticosterone (B), the natural glucocorticoid product of rats, suppressed endogenous B production of isolated rat adrenocortical cells induced by alpha ACTH-(1-24), [9-tryptophan (O-nitrophenylsulfenyl)]ACTH-(1-24) [( Trp (Nps)9]ACTH-(1-24], and cAMP as well as pregnenolone supported-steroidogenesis. This self-suppression occurred within 2 h. It was dependent on the concentration of exogenous B. However, self-suppression did not alter the half-maximal steroidogenic concentration (ED50) of each steroidogenic agent. In addition, exogenous B did not suppress ACTH-induced cAMP production or gross protein synthesis, as measured by leucine incorporation into bulk cellular proteins. These results with isolated cells suggested at least two mechanisms for self-suppression: 1) exogenous B inhibited steroidogenic steps in a noncompetitive manner, and/or 2) exogenous B induced B degradation. In this study we examined the effect of exogenous B on the degradation of B. Accordingly, we measured the adrenal 5 alpha-reductase activity (5 alpha RA) of cell homogenates prepared from treated cells. Isolated adrenocortical cells were incubated for 2 h with alpha ACTH-(1-24), ovine PRL (oPRL), and B. They were then homogenized and assayed for 5 alpha RA, as indicated by the disappearance of exogenous B, as shown by RIA. In addition, the percentage of exogenous tritium-labeled B [( 3H]B) converted to 5 alpha-dihydrocorticosterone (DHB), the principal reduced metabolite of B, was determined by TLC. Isolated adrenocortical cells from intact rats showed insignificant 5 alpha RA and DHB formation when incubated with or without alpha ACTH-(1-24) and with or without oPRL. However, with exogenous B, there was significant 5 alpha RA and DHB formation. oPRL plus B decreased DHB formation. The effects of B and oPRL were more demonstrable with cells from hypophysectomized rats. These cells exhibited high 5 alpha RA and DHB formation; exogenous B increased these values, whereas oPRL acutely reversed the effects of hypophysectomy and exogenous B. In other work avoiding cell homogenization, exogenous B suppressed ACTH-induced B accumulation and increased DHB formation in intact cell suspensions from intact rats and intact male domestic fowl. Furthermore, exogenous B increased the conversion of [3H] pregnenolone to DHB in intact cell suspensions from intact rats, showing that B synthesized de novo as well as exogenous B can be degraded during self-suppression. These data indicate that acute self-suppression of corticosteroidogenesis is at least partly mediated by an increase in 5 alpha RA.

Adrenal Cortex↗

Brain sites involved in the regulation of growth hormone secretion in the young male domestic fowl.

To study brain sites involved in the regulation of GH secretion in the domestic fowl, lesions were placed in and around the hypothalamus of 1-week-old cockerels. Circulating concentrations of GH were then measured at weekly intervals for 4 weeks after the placement of lesions. At the termination of the experiment, histological procedures were used to determine the exact site of the lesion in each bird. Although a fair degree of overlap existed between the lesion sites leading to stimulation and those causing an inhibition of GH secretion, a clear distinction could be made in the overall distribution of stimulatory and inhibitory sites of GH control. A high concentration of lesion sites resulting in GH decline (presumed GH-releasing factor-rich areas) appeared to reside in the general area of the ventromedial and the arcuate nucleus of the hypothalamus. Lesion sites causing a GH rise (presumed somatostatin-rich areas), on the other hand, seemed to have a more caudal distribution. In addition, some evidence of an anterior hypothalamic distribution of these presumed 'somatostatin' neurones was observed. These agree with the existing immunohistochemical data on the distribution of somatostatin and constitute experimental evidence for localization of presumed GH-releasing factor sites within the avian brain.

Animals↗

Effects of ovine growth hormone and other anterior pituitary hormones on lipolysis of rat and ovine adipose tissue in vitro.

Ovine growth hormone ( oGH ) was tested for its effects on lipolysis of rat and ovine adipose tissue in vitro. Ovine growth hormone at 1, 5 and 25 micrograms/ml stimulated lipolysis (P less than .05) of chopped rat adipose tissue and isolated rat adipocytes incubated in the presence of 100 mU/ml adenosine deaminase and .2 micrograms/ml dexamethasone, but had no effect on lipolysis of chopped ovine adipose tissue or isolated ovine adipocytes. Isoproterenol, a beta-adrenergic agonist, stimulated lipolysis (P less than .05) of both rat and ovine adipose tissue. Contaminants of the oGH preparation used were examined for lipolytic effects. Thyroid-stimulating hormone (TSH), luteinizing hormone (LH) and adrenocorticotropic hormone (ACTH) content in oGH were measured by radioimmunoassay. When quantities of these hormones contaminating 5 and 25 micrograms oGH were tested for lipolysis in rat adipose tissue, the TSH contamination could account for some (30%) of the lipolysis observed with oGH , while the other hormones had no effect. Also, preincubation of oGH with anti-GH, but not with anti-TSH or anti-LH, removed the principle in oGH responsible for the lipolytic effect on rat adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Enhanced growth and immune development in dwarf chickens treated with mammalian growth hormone and thyroxine.

The effects of growth hormone and/or thyroxine treatments on antibody production, primary lymphoid organ development, and general body growth were examined in two dwarf strains (sex-linked dwarf--SLD, and autosomal dwarf--ADW) and in a normal-growing strain (K) of White Leghorn chickens. One-day-old male chicks were assigned to experimental groups and were treated either with thyroxine (T4) feed supplements or daily mammalian growth hormone (GH) injections or a combination of these treatments (T4/GH). Within the SLD strain, GH treatments resulted in a significant enhancement (P less than 0.005) of humoral immune responsiveness and bursal growth while T4 treatments significantly (P less than 0.05) stimulated thymic growth. Overall growth in the SLD was also stimulated by T4 treatments. GH and/or T4 treatments had no specific effects on primary lymphoid organ growth in the ADW strain but either treatment separately resulted in a significant (P less than 0.05) increase in overall body size. None of the treatments significantly (P greater than 0.05) affected any of these parameters in the K-strain controls. Supplementation with T4 significantly elevated serum T4 levels within all strains. There were, however, no significant differences in the serum levels of T4 between strains within any of the treatment groups. Serum triiodothyronine (T3) levels were significantly lower in all treatment groups of the SLD as compared to the K-strain control. ADW serum T3 levels were significantly lower than the K-strain only in the T4-treated group. No differences (P greater than 0.05) were found between the dwarf and control strains in endogeneous GH levels, although mammalian GH treatments did produce significant changes in serum T3 and T4 levels within the K-strain. These results provide evidence that hormonal manipulations can significantly affect body growth, primary lymphoid organ development, and immune function in the dwarf strains studied and suggest these strains may be useful models for future studies on hormonal interactions and immune function.

Animals↗

Effects of triiodothyronine treatments on body and organ growth and the development of immune function in dwarf chickens.

The effects of triiodothyronine (T3) treatments on general body growth, long bone growth, primary lymphoid organ development, antibody production, and serum growth hormone (GH) and thyroid hormone levels were examined in two dwarf strains (sex-linked dwarf--SLD, and autosomal dwarf--ADW) and in a normal-growing control strain (K) of White Leghorn chickens. One-day-old male chicks from each of these strains were assigned to either an untreated control group or to one of the groups receiving a T3 supplement ranging from 0.01 to 1.0 ppm. General body growth and long bone growth were significantly (P less than 0.05) stimulated only within the SLD strain by the intermediate T3 dosages. The 1.0-ppm T3 dosage level resulted in depressed body weights within both the K and ADW strains but produced no significant changes within the SLD strain. Thymic growth was significantly stimulated due to treatments of 0.1 ppm T3 in the SLD strain (P less than 0.05) and 1.0 ppm T3 in both the SLD and ADW strains (P less than 0.001 and P less than 0.05, respectively). Bursal growth was significantly depressed (P less than 0.05) at all T3 dosage levels within the SLD strain while 0.01 and 0.1-ppm T3 treatments resulted in significant bursal growth stimulation in the K and ADW strains, respectively. Concomitant with the depressed bursal growth, antibody production was significantly depressed (P less than 0.05) within the SLD strain at the 1.0-ppm T3 dosage level. Antibody production was not significantly affected by any of the T3 treatments within the control K or ADW strains. Serum T3 levels were significantly increased in all strains by the T3 supplementation but thyroxine (T4) serum levels were affected only within the SLD strain. The 0.01-ppm T3 treatment resulted in a significant increase (P less than 0.05) in serum T4 levels within this strain and treatment group. The only increase (P less than 0.05) in GH levels due to T3 treatments occurred within the same SLD treatment group. The higher T3 treatments resulted in serum GH levels being severely depressed (P less than 0.01) in all strains.

Animals↗

Two avian luteinizing hormone radioimmunoassay procedures compared by measurement of changes during the ovulatory cycle of turkey and broiler hens.

Two radioimmunoassay (RIA) procedures for measuring avian luteinizing hormone (LH) were compared using divided aliquots of plasma samples collected during the ovulatory cycles of turkey and broiler breeder hens in three separate experiments. The RIA systems compared were the homologous turkey LH assay Wentworth et al. (1976) and the homologous chicken LH assay of Follett et al. (1972). Both assays provided the same assessment of circulating LH changes. The preovulatory surge of LH was observed 6 hr before ovulation in turkeys and 4 hr before ovulation in chickens. In addition, both assays detected an increase in chicken LH after ovulation, followed by a gradual decline prior to the next preovulatory surge. The correlation between RIA were highly significant (P less than .001) in each experiment. The crossreaction of purified ostrich LH, FSH, and TSH and of the alpha and beta subunits of turkey LH was assessed in each assay system. Ostrich LH, FSH, and TSH crossreacted in the chicken LH assay in a dose-related manner: ostrich LH showed the highest activity. Only ostrich TSH produced a response in the turkey assay that was dose related. The alpha subunit, but not the beta subunit, of turkey LH was quite potent in the chicken LH RIA, but neither subunit competed as well as the native hormone in the turkey RIA. Thus, the two LH antisera recognize different portions of the LH molecule. The chicken antiserum apparently recognizes a site on the alpha subunit that may be at least partially masked in the FSH and TSH molecules. The turkey antiserum recognizes a site on the native LH molecule that is altered when the subunits are separated.

Animals↗

Hormones and growth in poultry.

The hormonal control of growth in poultry and other species is complex. The available evidence supports the concept that growth hormone and the thyroid hormones are the principal hormones responsible for the attainment of normal growth in the domestic fowl. Other hormones, including somatomedins, epidermal growth hormone, sex steroids, and vitamin D metabolites, are also involved in the control of growth. Considerable study will be required for the elucidation of the exact roles of the various hormones in avian growth.

Adrenal Cortex Hormones↗

Seasonal changes in circulating levels of luteinizing hormone and growth hormone in the migratory Canada goose.

Seasonal changes in plasma levels of LH and GH in the Canada goose (Branta canadensis interior) have been studied. The population examined breeds in the Canadian subarctic region (Fort Churchill, Manitoba) and winters in the southern United States (Swan Lake Refuge, Missouri). Peak levels of LH were observed during spring postmigratory (nestbuilding, early May) and nesting (incubating, early June) periods, while no significant differences were observed during the other periods studied. The highest levels of GH were observed during molting (late July) and the immediately following fall premigratory (early September) period.

Animals↗

Pharmacological studies on the noradrenergic control of luteinizing hormone secretion in the domestic fowl.

A neuropharmacological approach was utilized in order to investigate catecholaminergic involvement in the control of LH secretion in the domestic fowl. Inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine (alpha Mpt) at several doses was accompanied by significant reductions in the circulating LH concentration of 6-week-old male cockerels. Plasma LH was similarly depressed following the selective inhibition of NE synthesis by either diethyldithiocarbamate (DDC) or FLA 63. Blockade of alpha 1-adrenergic receptors with phenoxybenzamine was consistently associated with precipitous declines in plasma LH concentrations. Stimulation of alpha-adrenergic receptors by phenylephrine and clonidine elevated circulating LH levels. Activation of the dopaminergic system by apomorphine depressed LH release. However, pimozide was without effect. These data suggest that norepinephrine is involved in the stimulation of LH release, while dopamine may exert an inhibitory influence. Evidence of some stimulatory beta-adrenergic effect is also described.

Animals↗

Effects of glucocorticoids on circulating concentrations of thyroxine (T4) and triiodothyronine (T3) and on peripheral monodeiodination in pre- and post-hatching chickens.

The administration of either glucocorticoids (dexamethasone or corticosterone) or adrenocorticotropic hormone (ACTH) to chicken embryos was followed by increase in the circulating concentration of triiodothyronine (T3), the T3 to thyroxine (T4) ratio and the activity of liver T4-5' monodeiodinase. No consistent changes in plasma concentrations of T4 or GH were observed. In post-hatching chicks, corticosterone and dexamethasone depressed the circulating concentrations of both T4 and T3. Iopanoc acid, an inhibitor of liver T4-5' monodeiodinase, elevated plasma concentrations of T4 and depressed those of T3 in both chicken embryos and young chicks. It is suggested that glucocorticoids affect circulating concentrations of T4 and T3 both by affecting the activity of the liver T4-5' monodeiodinase and by influencing the hypothalamo-pituitary axis.

Adrenocorticotropic Hormone↗

Effect of a tryptophan deficiency on thyroid gland, growth hormone and testicular functions in chickens.

Broiler chicks from 2 to 4 weeks of age were fed control (0.23%) and deficient (0.115, 0.058%) levels of L-tryptophan. Separate groups of control chicks were pair-fed daily with the deficient chicks. Deficient chicks grew less efficiently than did pair-fed controls. Plasma triiodothyronine (T3) was elevated in deficient chicks, especially compared to pair-fed controls, and this was accompanied by lower reverse T3. Plasma thyroxine (T4) was also reduced with 0.059% tryptophan. However, thyroid weights and follicle diameters were unchanged. Reductions in weight gain and bone growth, increases in pituitary and pineal weights, and elevations in plasma GH occurred in the tryptophan-deficient chicks apart from any effect due to reductions in feed intake. Comb and testis size, and plasma testosterone were little affected by the deficiency. Based on changes in plasma T3 levels and feed conversion efficiencies, we conclude that tryptophan-deficient chicks show signs of relative hyperthyroidism and energy wastage compared to pair-fed controls. The elevations in plasma growth hormone and T3 support the concept that serotonin is a negative modulator of the synthesis or release of these hormones in chickens.

Animals↗

Variation in the release of thyroxine, triiodothyronine and growth hormone in response to thyrotrophin releasing hormone during development of the domestic fowl.

In newly hatched chicks, TRH administration was followed by increased circulating concentrations of growth hormone (GH), thyroxine (T4) and 3,3',5-triiodothyronine (T3). Little change in the circulating concentration of 3,3',5'-triiodothyronine (rT3) was however observed. The effect of TRH on the circulating concentration of GH was not found in chick embryos at 17 or 19 days of incubation but was observed during pipping. The T4 response was maximal in newly hatched chicks and present in 17 and 19 days embryos. The magnitude of the T3 responses increased with age while that of T4 decreased.

Age Factors↗

Abnormalities in the plasma concentrations of thyroxine, tri-iodothyronine and growth hormone in sex-linked dwarf and autosomal dwarf White Leghorn domestic fowl (Gallus domesticus).

Plasma concentrations of GH were high in young birds (2-12 weeks old) and low in older birds (15 and 18 weeks old) in the control Cornell K strain of White Leghorn fowl. There was little variation in the plasma concentrations of tri-iodothyronine (T3) and thyroxine (T4) with age in this strain. Similar patterns of plasma hormone concentrations with age were observed in autosomal recessive dwarf chickens. However, the plasma concentrations of T3 and T4 tended to be depressed while that of GH was raised. There was little age-related change in the plasma concentrations of GH, T3 and T4 in sex-linked recessive dwarf chickens. Throughout growth and maturation the plasma concentrations of T3 in the sex-linked dwarf birds were less 40% of those observed in the control strain. Plasma concentrations of T4 tended to be raised relative to the control in the sex-linked dwarf at each age examined. The plasma concentration of GH was raised only in older (12, 15 and 18 weeks old) sex-linked dwarfs. Liver T4-5' monodeiodinase activity was slightly depressed in autosomal dwarf chickens and very low in the sex-linked dwarf fowl. Neither autosomal nor sex-linked dwarfism appears to be due to hypopituitarism. It is probable that the depressed liver 5' monodeiodinase activity and the concomitant low plasma concentrations of T3 are a causative factor in the reduced growth and stature of the sex-linked dwarf chicken.

Animals↗

Influences of growth hormone on glucose uptake by avian adipose tissue.

The uptake of glucose by chicken adipose tissue was determined in vitro using adipocytes or adipose explants using 14C orthomethyl glucose (OMG). The net uptake of 14C-OMG was enhanced by preparations of bovine and chicken GH and by insulin. Insulin and growth hormone (GH) (chicken or bovine) stimulated the uptake of 14C-OMG occurring in 1 hr by adipose tissue (both adipocytes and explants) from chicks hypophysectomized for 5 days but not from sham-operated birds. Tissue preincubated with GH became refractory to GH stimulation of 14C-OMG uptake. The short-term (2 to 15 min) uptake of 14C-OMG by explants was, however, stimulated by the bovine GH and insulin in tissue from sham-operated but not hypophysectomized chicks. Surprisingly, net decreases in 14C-OMG uptake, in the presence of bovine GH, were observed with adipose tissue (adipocytes and explants) from hypophysectomized birds, when incubated in the presence of epinephrine, and from hypophysectomized birds immediately following surgery.

3-O-Methylglucose↗

Steroidogenic and morphological responses of hen granulosa cells to luteinizing hormone in vitro.

We examined in vitro progesterone production in granulosa cells isolated from the first (F1 group, 35 mm diameter) and third (F3 group, 25 mm diameter) largest ovarian follicles and granulosa cells isolated from hens stimulated hormonally to produce multiple follicular maturation (PMSG group). All granulosa cell groups maintained in a 48 hr culture produced progesterone. Luteinizing hormone (LH) significantly increased progesterone production for each group with the PMSG group progesterone levels the highest and F3 group the lowest. Light and scanning electron microscopy revealed that few single granulosa cells were present after 48 hr culture. Instead, granulosa cells were observed as multicellular aggregates, referred to here as clusters, which ranged between 15 and 60 micron in diameter. Regardless of the cell group few clusters attached to a support surface. The surface of F1 and PMSG clusters were irregular due to short folds and formed few surface elaborations. Individual cell boundaries within a cluster could not be discerned. With LH, surface folds became more elaborate, often giving rise to microvilli. Blebs about 1 micron in diameter or less also were more prevalent on clusters from groups cultured with LH. Clusters within the F3 group cultured with and without LH were similar in appearance. Therefore, in the F1 and PMSG groups, the development of surface elaborations in the form of microvilli and blebs was correlated with the LH promoted increase in progesterone production.

Animals↗