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Biomedical subjects

S Edén

Publications and source records attributed to S Edén.

At least 109 records · Page 6Linked to original sources
PubMed1983

Relationship between the biological and immunological activities of growth hormone circulating in normal rats.

The ability of GH to induce refractoriness to its own insulin-like effect in adipose tissue is highly specific for GH. Moreover, refractoriness to the insulin-like action of GH can be induced with low concentrations of GH in the range of 10 ng/ml. In the present study, the ability of plasma from normal rats to induce refractoriness to the effect of GH on the production of 14CO2 from [14C]glucose in epididymal fat pads from hypophysectomized rats was examined as a measure of a GH-specific biological effect of the plasma. Plasma levels of GH were measured by RIA. Without exception, preincubation of fat pads with plasma having immunoreactive rat GH (rGH) levels over 50 ng/ml induced refractoriness to GH, whereas plasma having immunoreactive rGH levels below 15 ng/ml did not exert this effect. In fat pads preincubated with plasma having immunoreactive rGH levels between 10-50 ng/ml, the effect of a second exposure to GH varied in a dose-dependent manner. Also, plasma pools that were diluted with buffer or plasma from hypophysectomized rats were unable to induce refractoriness when the calculated or measured levels of immunoreactive rGH were below 15 ng/ml. The results suggest that in terms of the ability of GH to induce refractoriness to the insulin-like effect of the hormone, a very good correlation exists between the biological and immunological activities of GH in plasma from normal undisturbed rats.

Adipose Tissue↗
PubMed1982

Ability of growth hormone fragments to complete with 125I-iodinated human growth hormone for specific binding to isolated adipocytes of hypophysectomized rats.

Several noncovalent complexes of large fragments of human GH, which are less active than native human GH in stimulating glucose metabolism in adipose tissue of hypophysectomized rats, were tested for their ability to compete with 125I-iodinated human GH for specific binding to isolated adipocytes of hypophysectomized rats. The complexes tested were A (residues 1-134 + residues 141-191; S-carbamidomethylated), B (residues 1-134 + residues 135-191; S-carbamidomethylated) and C (residues 1-134 + residues 135-191; S-carboxymethylated). When compared to native human GH, the complexes were less active in competing with 125I-iodinated human GH for specific binding to adipocytes, and their order of potency in the binding assay (A greater than B greater than C) was similar to that of their respective activities in stimulating glucose metabolism in isolated adipose tissue of hypophysectomized rats.

Adipose Tissue↗
PubMed1982

Up- and down- regulation of central postsynaptic alpha 2 receptors reflected in the growth hormone response to clonidine in reserpine-pretreated rats.

The alpha-adrenergic mechanisms exert a stimulatory influence on the secretion of growth hormone (GH) in the rat. In the present study the alpha receptors involved in GH regulation were characterized with respect to subtype. It was also investigated whether the GH response to alpha receptor agonists can be utilized to assess change in the responsiveness of central alpha receptors. The experiments were performed on rats with implanted intra-aortic cannulae allowing frequent blood sampling from freely moving animals. Plasma GH was determined by radioimmunoassay. Reserpine (10 mg/kg) caused a suppression of the normal pulsatile secretory pattern of GH. The alpha receptor agonist clonidine (CLON) given to reserpine-pretreated animals induced a dose-dependent increase in plasma GH. The effect of CLON (0.2 mg/kg) was prevented by pretreatment with the alpha 2 receptor antagonist yohimbine (3 mg/kg), but not by the alpha 1 receptor antagonist phenoxybenzamine (10 mg/kg). Chronic pretreatment with CLON or imipramine, either of which can be expected to produce a reduced sensitivity of central alpha 2 receptors, resulted in reduced GH responses to CLON. On the other hand, chronic treatment with yohimbine, which should cause denervation supersensitivity of alpha 2 receptors, led to enhanced GH responses to CLON. The results indicate that GH release in the rat is stimulated by postsynaptic alpha 2 receptors. They also suggest that the GH response to CLON can be used as a valid in vivo model reflecting decreased, as well as increased responsiveness of this type of receptor.

Animals↗
PubMed1982

Effects of gonadectomy and testosterone replacement on growth hormone response to alpha 2 adrenergic stimulation in the male rat.

The growth hormone (GH) response to clonidine in reserpine-pretreated rats is a putative in vivo model to reflect activation of central postsynaptic alpha 2 receptors. In the present study the influence of testosterone on the responsiveness of central alpha 2 receptors was investigated using this method. One week after operation the GH response to clonidine was drastically reduced in gonadectomized adult male rats compared to sham-operated controls. Testosterone replacement completely antagonized the effect. The results suggest an influence of testosterone on central postsynaptic alpha 2 receptors or on structures connected to these receptors.

Animals↗
PubMed1982

Effect of frequency of growth hormone administration on longitudinal bone growth and body weight in hypophysectomized rats.

The effect of frequency of growth hormone (GH) administration on longitudinal bone growth and body weight was studied in hypophysectomized rats. Replacement therapy with 3 different doses of human GH [(hGH) Crescormone] was started 10-14 days after hypophysectomy and was continued for 5 days. Longitudinal bone growth, as measured by the tetracycline method, and body weight were determined during the injection period. With a daily replacement dose of 128 micrograms of hGH body weight gain and longitudinal bone growth were significantly higher when the hormone was injected 4 and 8 times per day compared with animals receiving the hormone in one daily injection. When the dose of hGH was 32 or 8 micrograms per day, longitudinal bone growth and body weight gain were more pronounced in animals receiving the hormone 2 and 4 times per day compared with animals receiving the hormone one or 8 times per day. The results of the present study demonstrate that the frequency of GH administration influence body growth. The findings suggest that the secretory pattern of GH influence the growth rate under in vivo condition.

Animals↗
PubMed1982

Circumstantial evidence for a role of the secretory pattern of growth hormone in control of body growth.

The effect of frequency of growth hormone (GH) administration on longitudinal bone growth and body weight was studied in hypophysectomized rats which were given replacement therapy with corticosteroids, thyroxine and GH with start of therapy on the day of surgery. Longitudinal bone growth, as determined by the tetracycline method, was measured during the last 5 days of the 9 day long period with replacement therapy. The daily replacement dose of GH (bGH-17:NIH) was 200 micrograms and was given on 1, 2, 4 or 8 occasions. Longitudinal bone growth was enhanced in the groups of animals receiving the hormone on two or more occasions per day. The most pronounced response was seen with an administration frequency of four times per day. Changes in body weight during the injection period showed similar changes. The results of the present study show that the administration frequency of growth hormone is important for the growth rate in hypophysectomized rats which have been given replacement therapy. The findings suggest that the secretory pattern of GH is an important factor for optimum growth.

Animals↗
PubMed1981

Effects of hypophysectomy, adrenalectomy and (-)-propranolol on ethanol-induced decrease in plasma amino acids.

In previous studies we have demonstrated that an acute dose of ethanol cause an immediate decrease in most plasma amino acids in both man and rat. This effect of ethanol is partly inhibited by the beta-adrenergic antagonist (-)-propranolol, partly by adrenalectomy or hypophysectomy and almost completely by a combination of adrenalectomy with (-)-propranolol. This finding suggests an involvement of both beta-adrenergic mechanisms and steroids from the adrenal cortex in the ethanol-induced decrease in plasma amino acids.

Adrenalectomy↗
PubMed1981

Importance of norepinephrine alpha 2-receptor activation for morphine-induced rat growth hormone secretion.

The normal pulsatile secretion of rat growth hormone (rGH) requires intact function in monoaminergic neurons. The importance of norepinephrine (NE) for the secretion is well documented, while the roles of dopamine (DA) and 5-hydroxytryptamine (5-HT) are still a matter of controversy. Morphine, as well as endogenous opioid peptides, are known to stimulate the secretion of GH. Whether the opiate-induced GH release is dependent on monoamines was investigated in the present study. Administration of morphine (10 mg/kg) resulted within 30 min in elevations of plasma rGH exceeding 40 ng/ml. This effect was almost completely antagonized by reserpine (10 mg/kg), given 5 h before morphine and partially antagonized by reserpine (2 mg/kg) administered 25 h before morphine. Administration of tetrabenazine (75 mg/kg) protects monoamine granules from irreversible destruction and counteracted the morphine antagonistic effects of reserpine (2 mg/dg) on rGH secretion indicating that the latter effect is due to blockade of monoaminergic neurotransmission. Pretreatment with either haloperidol (1 mg/kg), p-chlorophenylalanine (PCPA) (300 mg/kg x III) or phenoxybenzamine (10 mg/kg) did not reduce the effect of morphine on rGH release whereas yohimbine (3 mg/kg) effectively prevented it. In reserpine-pretreated animals administration of clonidine (0.5 mg/kg) potentiated the GH releasing effect of morphine. These results indicate that morphine-induced GH release is dependent on activation of postsynaptic NE receptors of the alpha 2-subtype.

Animals↗
PubMed1980

Enhanced growth hormone response to clonidine in the spontaneously hypertensive rat.

Plasma concentrations of growth hormone (GH) were measured after administration of clonidine (0.5 mg/kg) to spontaneously hypertensive (SH) rats and normotensive Wistar Kyoto controls. All rats were pretreated with reserpine (10 mg/kg). The GH response to clonidine was significantly higher in SH rats than in controls, indicating that in SH rats the responsiveness of post-synaptic alpha-adrenergic structures in the hypothalamus may be increased.

Animals↗
PubMed1979

In vitro effects of growth hormone on protein synthesis and amino acid transport in the rat diaphragm after acute hypophysectomy.

The effects of growth hormone (GH) in vitro on phenylalanine-14C incorporation to assess protein synthesis and on alpha-aminoisobutyric-1-3H accumulation to measure amino acid transport in the diaphragm muscle of the rat were investigated 2, 6 and 24 h after hypophysectomy or sham-operation. In hypophysectomized animals protein synthesis was depressed. GH in vitro was without effect 2 h after hypophysectomy but stimulated protein synthesis 6 and 24 h after the operation. Six hours after hypophysectomy amino acid transport was enhanced and further stimulated by GH. After 24 h amino acid transport was depressed but was stimulated to normal levels by GH. Six hours after sham-operation protein synthesis was depressed, but was stimulated by GH. After 24 h protein synthesis was normalized and GH was without effect. GH did not influence amino acid transport after sham-operation. Plasma levels of GH were undetectable after hypophysectomy, markedly depressed 2 and 6 h after sham-operation, but normal after 24 h. It is concluded that tissue responsiveness to GH develops a few hours after hypophysectomy.

Amino Acids↗
PubMed1979

Monoaminergic control of episodic growth hormone secretion in the rat: effects of reserpine, alpha-methyl-p-tyrosine, p-chlorophenylalanine, and haloperidol.

The effects on GH secretion of reserpine, alpha-methyl-p-tyrosine (alpha-MT), p-chlorophenylalanine (PCPA), and haloperidol were studied in undisturbed, unanesthetized male rats with implanted intraaortic cannulae. The effects of the various drug treatments on motor activity and brain levels of catecholamines (CAs) and 5-hydroxytryptamine (5-HT) as well as the synthesis of the biogenic amines were also studied. Reserpine (10 mg/kg, ip) completely inhibited GH secretion for at least 15 h. Repeated injections of reserpine prolonged this inhibition. Episodic GH secretion reappeared 36 h after the last administration of reserpine, at which time the behavioral inhibition and blepharospasm induced by the drug was less pronounced than after 24 h, but brain levels of CAs and 5-HT were still markedly reduced. Administration of alpha-MT (150 mg/kg; 12, 4, and 2 h before experiments) inhibited episodic GH secretion and caused marked inhibition of motor activity and brain levels of CAs but not 5-HT. The inhibition of episodic GH secretion was more pronounced with haloperidol (0.5 mg/kg; 30 min before experiments) than with alpha-MT but was not as complete as that found 12 h after administration of reserpine. Administration of p-chlorophenylalanine (300 mg/kg; 72, 48, and 24 h before experiments) had no effect on episodic GH secretion, whereas brain levels of 5-HT and 5-HT synthesis were markedly reduced.

Animals↗