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SUMMARY
The effects of adrenaline, noradrenaline, corticotrophin (ACTH), cortisol and corticosterone on the levels of blood lipids have been studied in dogs and rats. Blood glucose, plasma free fatty acids (FFA) and corticosteroids were determined 4 hr. after injection. Plasma cholesterol, phospholipids and triglycerides were determined 24 hr. after the last of three daily treatments. In some experiments an oral glucose load was given at the same time as the hormones. In dogs plasma FFA were increased by adrenaline and noradrenaline, decreased by ACTH plus glucose and not affected by ACTH alone. Gradual rises in the lipoprotein levels of dogs were produced by any of the hormones given and followed acute rises in corticosteroid concentration regardless of the acute changes in plasma FFA. In rats plasma FFA were increased by adrenaline and ACTH, decreased by glucose and not affected by ACTH plus glucose. It was not possible to produce rises in lipoprotein by administering adrenaline or ACTH to rats. Exogenous corticosteroids produced increases in the cholesterol and phospholipid levels. The effects of corticosterone were potentiated by oral glucose but cortisol produced a full effect without extra glucose. The FFA responses to subcutaneous adrenaline in rats were reduced by adrenalectomy, but the increases in plasma FFA produced by intravenous infusion of adrenaline or ACTH were similar in adrenalectomized and intact rats. It was concluded that changes in lipoproteins are not causally related to increased mobilization of FFA but are dependent on increased adrenocortical hormone secretion in the presence of excess carbohydrate.
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SUMMARY
Handling of intraperitoneal injections of saline, twice daily for 10 days, did not significantly affect the resting level of corticosterone in the plasma or the adrenals. The conditioning abolished the usual changes in corticosterone levels caused by further handling or injections, reduced the response to exposure to ether vapour and had no effect on the response to histamine. The effect of pentobarbitone on plasma and adrenal corticosterone concentrations was found to be dependent upon the state of the pituitary-adrenal system before administration. Pentobarbitone had no effect on the responses of the adrenal cortex to exogenous adrenocorticotrophin. The responses to ether vapour or histamine of normal rats and rats lightly sedated with pentobarbitone were not significantly different as judged by changes in plasma and adrenal corticosterone concentrations and adrenal ascorbic acid depletion. However, rats deeply anaesthetized with pentobarbitone gave responses indicative of a depression of pituitary-adrenal activity. The sites of action of pentobarbitone on the pituitary-adrenal system are discussed.
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SUMMARY
The concentration of corticosterone in the plasma of rats has been determined by a spectrophotofluorimetric method.
Animals housed in single cages, undisturbed for 18 hr. prior to testing show reproducible levels of 5·5 μg./100 ml. plasma. Rats housed in groups of 20 under the same conditions exhibit mean levels of 9·5 μg./100 ml.
Non-specific stimuli such as environmental change, noise, handling, weighing and intraperitoneal injections all produce marked increases in plasma corticosterone levels which remain supernormal for at least 2 hr.
The variation in the literature reports of 'resting' plasma corticosterone levels is discussed in the light of the present findings.
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SUMMARY
Changes in the concentration of ACTH in the plasma of normal and adrenalectomized rats subjected to mock adrenalectomy were studied at various time intervals after the operations. The time relationships of the changes in ACTH concentration in the plasma of both groups of animals were similar. The possible significance of the findings is discussed.
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SUMMARY
The concentration of ACTH in the plasma of both normal and adrenalectomized rats appears to be less than 5 milliunits/100 ml.
The results suggest, but do not prove, that the levels of adrenocorticotrophin were identical in the two groups of animals.
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Goldfish showed a significant reduction in their plasma sodium and calcium levels 1 h after receiving 50 i.u. calcitonin per kg body weight. When 100 i.u. calcitonin were injected there was a significant fall in circulating levels of both sodium and calcium and also of chloride ions compared with those found in untreated control animals. Administration of calcitonin to immature eels adapted to either freshwater or seawater conditions showed no significant change in plasma ion composition at doses of 10 i.u. per kg body weight or less. However, doses of 50 and 100 i.u. caused significant reductions in plasma sodium, chloride and calcium ion levels compared with sham-injected control animals.
When immature eels were given 100 i.u. calcitonin per kg body weight there were significant reductions in the plasma levels of sodium, chloride and calcium ions but the timing of these changes was slightly different. In freshwater-adapted eels, the depression of plasma sodium was seen after 30 min and lasted for up to 2 h, whilst depression of plasma chloride and calcium was not seen until 1 h after injection. In addition, whilst the lowering of plasma chloride ions lasted up to 2 h after injection, the plasma calcium had returned to the preinjection control level by this time.
In seawater-adapted eels the depression of sodium, chloride and calcium levels was seen at 30 min and the effect continued for up to 2 h after injection when the depression was no longer apparent.
