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S Edén

Publications and source records attributed to S Edén.

115 records · Page 7Linked to original sources
PubMed1978

Plasma levels of growth hormone in female rats of different ages.

Radioimmunoassayable growth hormone (GH) was determined in fed and fasted female rats of different ages. In 6-40 day-old rats blood was collected at hourly intervals in groups of rats at different time intervals during the day. Within each age group the variation in plasma GH was considerable. In 6-14 day-old rats plasma GH was generally elevated. By day 18 levels declined, lowest on day 22 and by day 26 again increasing. In 14 day-old rats the median plasma level of GH was 22 ng/ml, in 22 day-old rats less than 5 ng/ml and in 40 day-old rats 43 ng/ml. In 14 day-old rats levels ranged from less than 5 ng/ml--148 ng/ml, in 22 day-old rats from less than 5 ng/ml--34 ng/ml and in 40 day-old rats from less than 5 ng/ml--greater than 200 ng/ml. A 20 h fasting period was associated with a significant decrease in plasma GH. In 45 day-old rats, the variations in plasma GH of individual animals were studied by obtaining sequential blood samples from unrestrained, undisturbed animals with implanted intra-aortic cannulae. In these rats GH secretion was characterized by an episodic release, occurring every 2--4 h. After a 20 h fasting period major peaks were depressed and occurred less frequently. It is concluded that there is an age-related as well as a circadian rhythm in growth hormone secretion in the rat and that sequential sampling of blood is essential for the evaluation of the secretory pattern.

Aging↗
PubMed1977

Effect of insulin and adrenaline on cyclic AMP in the diaphragm of normal and diabetic rats.

The effects of insulin and adrenaline on cyclic AMP (cAMP) levels in diaphragms of normal, streptozotocin-diabetic and insulin-treated diabetic rats were studied. Adrenaline caused a biphasic rise in cAMP with peak values of cAMP within the first few minutes. Diaphragms of diabetic rats showed an increased responsiveness to adrenaline. Injection of insulin to diabetic rats normalized the rise in cAMP after addition of adrenaline. There was no difference in basal levels of cAMP between diaphragms of normal, diabetic or insulin-treated diabetic rats. Insulin in vitro did not affect basal cAMP-levels or the release of cAMP from the tissue but significantly decreased adrenaline-induced peak levels of cAMP. This effect of insulin was abolished by theophylline. The results of the present study suggest that experimental diabetes is associated with changes of the adenylate cyclase and/or phosphodiesterase enzyme activities in skeletal muscle resulting in an increased responsiveness to adrenaline. Since insulin in vitro depressed the adrenaline-induced elevation of cAMP the increased responsiveness in diaphragms of diabetic rats might be attributed to the specific lack of insulin.

Animals↗
PubMed1976

Effect of adrenaline on the release of cyclic AMP by the rat diaphragm.

An investigation was made of the effect of adrenaline on the tissue level and release of cyclic AMP (cAMP) into the incubation medium by the isolated rat diaphragm preparation. Adrenaline, added in vitro, caused a dose-dependent biphasic increase in the tissue level of the nucleotide. A significant elevation of the level of cAMP in the tissue was observed throughout a 60 min incubation period in the presence of 0.01, 0.1 and 10 mug/ml of adrenaline. The hormone also produced a small but significant increase in the release of cAMP into the incubation medium. The accumulation of cAMP in the incubation medium ceased after 10 min of incubation in the presence of adrenaline, although the tissu e level of the nucleotide remained considerably elevated throughout the entire incubation period. Theophylline potentiated the effect of adrenaline on both the accumulation of cAMP in the tissue and in the incubation medium. Theophylline by itself also increased the tissue level of cAMP slightly. It is concluded from the present study that the elimination of cAMP from the rat diaphragm muscle by release of the nucleotide from the cells is small.

Animals↗
PubMedDate not supplied

Growth hormone stimulates the proliferation of cultured chondrocytes from rabbit ear and rat rib growth cartilage.

The effect of growth hormone (GH) on various growth processes is generally considered to be indirect, mediated by GH-dependent plasma factors--somatomedins--which are produced mainly in the liver. In vitro, somatomedins stimulate a number of processes that apparently are associated with cell growth. It has been difficult, however, to induce skeletal growth by the administration of somatomedins in vivo. Daily injections of a partially purified somatomedin preparation failed to induce accumulated longitudinal bone growth using the intravital marker tetracycline or by measuring the nose-to-tail length. Administration of insulin-like growth factor I (IGF I) which is probably identical to somatomedin C, to hypophysectomized rats has been reported to increase the width of the epiphyseal plate. But although this suggests an in vivo effect of IGF I on longitudinal bone growth, such an effect has not been directly demonstrated. Recently, we reported that local administration of human GH (hGH) into the proximal cartilage growth plate of the tibia of hypophysectomized rats stimulated longitudinal bone growth on the side injected with the hormone. Furthermore, we have identified specific binding sites for hGH in cultured chondrocytes from rabbit ear and epiphyses. Here, we show that hGH, but not the structurally related polypeptides ovine prolactin or human prolactin, stimulates DNA synthesis in chondrocytes from rabbit ear and from rat rib growth plate, cultured in a chemically defined medium without the addition of serum. Our results suggest that GH directly initiates proliferation in mammalian chondrocytes.

Animals↗