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During investigation of adrenocortical functions in marsupials, three young red kangaroos (Megaleia rufa, Desm.) weighing between 14·5 and 15·5 kg were bilaterally adrenalectomized in two stages, separated by 10–15 days, by the lumbar extraperitoneal approach during halothane anaesthesia. A vinyl catheter was implanted in a jugular vein for blood sampling.
Two animals were injected daily with 25 mg cortisol acetate (FAc) and 2·5 mg deoxycorticosterone acetate (DOCA) i.m., after the second stage of adrenalectomy. The third animal was given 25 mg FAc only. During the next 6 days, the plasma [Na+] of all three animals remained in the range 141 ± 4 (s.d.) mmol/l. The plasma [K+] of the former two animals remained within the limits 3·6–4·2 mmol/l; that of the FAc-treated animal rose from 2·8 to 6·8 mmol/l but then fell to 5·2 mmol/l 3 days after the dose of FAc was doubled. Withholding the daily injection of DOCA
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ABSTRACT
In a study of adrenocortical functions in macropodid marsupials, measurements were made of the effects of ACTH infusion, ether stress and adrenaline infusion on plasma corticosteroid and glucose concentrations in wallabies (Thylogale billardierii) provided with indwelling venous catheters.
The mean plasma total glucocorticoid concentration in undisturbed males and females was 80 ± 5 (s.e.m.) μg/l, of which more than 90% was cortisol. This fraction declined to 68% of the total at the highest ACTH-stimulated concentration of 225 μg/l, due to an increase in the contribution by 11-deoxycortisol.
Although maximal ACTH stimulation (4·5 i.u./kg per h) caused a five- to sixfold increase in cortisol secretion rate, as measured by isotope dilution during constant-rate tracer infusion, plasma cortisol concentration rose only two- to threefold, due to a marked increase in metabolic clearance.
Plasma glucose concentration did not change significantly during either short-term (1 h) i.v. infusion or long-term (8 days) i.m. injection of ACTH, even though plasma cortisol concentration was significantly increased.
Ether anaesthesia caused a marked hyperglycaemia that preceded an increase in plasma cortisol concentration and was not sustained while plasma cortisol concentration continued to increase.
Infusion of adrenaline i.v. at rates sufficient to cause a similar hyperglycaemia had no significant effect on plasma cortisol concentration. A marked hyperglycaemia during xylazine anaesthesia was not associated with an increase in plasma cortisol concentration and was attributable to suppression of insulin secretion.
It is concluded that, as in the red kangaroo (Macropus rufus) and the quokka (Setonix brachyurus) and in contrast to the reported effects in the tammar wallaby (Macropus eugenii), neither ACTH, nor the increase in plasma glucocorticoid concentration caused by ACTH administration, influence plasma glucose concentration in Thylogale billardierii.
J. Endocr. (1986) 110, 471–480
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ABSTRACT
In undisturbed pademelon wallabies (Thylogale billardierii) with indwelling jugular venous catheters, an increase in the plasma cortisol concentration from 0.25±0.05 to 1.35±0.15 (s.e.m.) μmol/l in 2 h, during i.v. infusion of cortisol at 1.0 mg/kg per h, caused no significant change in the plasma glucose concentration from the control value of 4.26±0.25 mmol/l. The rates of appearance (Ra) and metabolic clearance (MCR) of glucose, measured by steady-state isotope dilution, also did not change significantly from the control values of 14.9±0.7 μmol/kg per min and 3.52±0.19 ml/kg per min respectively. Twice-daily i.m. injections of 7 mg cortisol/kg for 7 days caused increases in plasma concentrations of cortisol, from 0.26±0.02 to 0.66±0.04 μmol/l on day 7, and glucose, from 5.1±0.1 to 7.2±0.6 mmol/l by day 5. The concentration of glycogen in the liver of wallabies fasted for 24 h increased from the control level of 1.17±0.56 to 5.92±1.14 g/100 g on day 7 (P<0.01), but mean glucose Ra and MCR did not change significantly. Plasma concentrations of α-amino nitrogen rose from 2.73±0.13 to 3.22±0.12 mmol/l on day 1 and remained at this level. Plasma concentrations of urea rose from 8.59±0.62 to 9.70±0.32 mmol/l on day 1, but then declined below the control level. Food intake and urinary excretion of nitrogen did not change in undisturbed animals. However, fasting followed by liver biopsy was accompanied by urinary excretion of nitrogen in excess of food intake, persisting until day 2 of treatment.
The transient effect of cortisol on the plasma concentration of urea and lack of effect on urinary excretion of nitrogen could be explained by urea recycling, as indicated by a low urinary urea nitrogen: total nitrogen ratio and failure to excrete more than a mean of 26% of infused urea.
It is concluded that cortisol has no short-term effect on carbohydrate metabolism in this marsupial. In the long term it can increase hepatic carbohydrate reserves through utilization of tissue amino nitrogen, the resulting urea being conserved by recycling.
J. Endocr. (1988) 116, 71–79
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SUMMARY
Using an enzyme kinetic technique, a substance with the properties of renin was assayed in extracts of kidney and peripheral blood from the Australian marsupial Trichosurus vulpecula. The renin concentration in peripheral venous plasma varied from 10 to 855 units/ml. and plasma renin activity from 1·0 to 3·6 ng. angiotensin/ml./hr. High plasma renin concentration and plasma renin activity was associated with an appetite for salt and were significantly reduced by ingestion of 0·9% NaCl solution. Animals with low renin levels did not have a salt appetite. Sodium deficiency caused by mercurial and non-mercurial diuretics increased plasma renin concentration and plasma renin activity, and induced an appetite for salt. Plasma renin concentration and plasma renin activity also increased after haemorrhage.
Granulation of juxtaglomerular cells, demonstrated with Bowie's stain, increased considerably during sodium deficiency.
It is concluded that T. vulpecula has the eutherian type of renin—angiotensin system.
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SUMMARY
In the marsupial Trichosurus vulpecula, the decay curve of plasma renin concentration against time, during a period of 4 hr. immediately after either bilateral nephrectomy or i.v. injection of a partially purified homologous renin, could be resolved into two exponential components. The curves in both types of experiment were similar, suggesting a simple twopool system of renin distribution. The half-times of the first and second components were 11·1 ± 2·6 (s.d.) and 217 ± 71·5 min. respectively.
As in dogs, the initial volume of distribution of injected renin was equivalent to approximately 10% of body weight. Using this value, and the derivative of the post-nephrectomy decay curve at the time of removal of the second kidney, the renin production rate at this time was calculated to be in the range of 123–1170 units/min. This calculation was justified by demonstrating that the surgical manipulations did not cause any increase in plasma renin concentration. Renal renin production rates, measured in other possums from the difference in renin concentrations of arterial and renal venous plasma, were within the range calculated from the postnephrectomy decay curves.
Metabolic clearance rates calculated from the post-nephrectomy decay curves averaged 3·5 ml./min./kg.; and those calculated from the post injection decay curves averaged only 1·9 ml./min./kg. Circulatory changes, due to nephrectomy or renin injection, are the most likely reasons for this discrepancy.
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SUMMARY
When exposed to a low ambient temperature of 5 °C, adrenalectomized echidnas were able to increase their metabolic rate and to maintain their body temperature within the normal range for no more than 48 h — less than 12 h in five out of six animals. Thereafter, activity, metabolic rate, cardiac rate and body temperature declined and the animals became torpid.
When maintained with daily i.m. injections of 1–2 mg cortisol acetate/kg, adrenalectomized echidnas maintained activity and normal body temperature in the cold environment indefinitely. When cortisol injections were withheld and exposure to cold continued, normal body temperature was maintained for a further 10 days, after which it declined rapidly.
The onset of torpor was always preceded by a marked fall in plasma glucose concentration, as occurred in normal, but fasted, echidnas after prolonged exposure to cold. Both cortisol and corticosterone have glucocorticoid activity in echidnas, and torpor was prevented in adrenalectomized echidnas by preventing the fall in plasma glucose with either intermittent injections or constant rate infusions of glucose solutions.
The adrenal glands of normal echidnas exposed repeatedly to low environmental temperatures showed marked hypertrophy and increase in lipid content.
It is concluded that adrenocortical secretions are necessary for the metabolic response to cold stress in these prototherian mammals, and a major role of the corticosteroids is in maintenance of normal blood glucose concentrations, presumably by enhancing hepatic gluconeogenesis.
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SUMMARY
Using the techniques of equilibrium dialysis at 36 °C and gel filtration at 4 °C, a highaffinity, transcortin-like, corticosteroid binding system has been demonstrated in the blood plasma of the marsupial Trichosurus vulpecula.
The affinity constant for non-albumin binding was 4·018 ± 1·032 × 107 (s.d.) 1/mol for males and 4·046± 0·981 × 107 for females. The concentration of non-albumin binding sites was 1·82 ± 0·76 × 10−7 mol/l in males and 1·86 ± 0·57 × 10−7 mol/l for females. Oestrogen administration, sufficient to cause marked hypertrophy of the genital tract in the females, had no effect on the affinity constant or the concentration of the non-albumin binding sites in either males or females.
The general condition of the animals deteriorated during oestrogen administration and there were significant falls in the concentrations of albumin and cortisol in the blood plasma. In one animal which died during oestrogen treatment, the adrenal glands were significantly hypertrophied.
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SUMMARY
Brush-tailed opossums were prepared surgically with indwelling hepatic and jugular venous catheters for blood sampling without disturbance in the conscious state.
Hepatic extraction of [125I]Rose Bengal was 21 ± 3 (s.d.)% and hepatic clearance, used as a measure of hepatic blood flow, was 42·5 ± 7 ml/kg/min. Hepatic release of new glucose, calculated from the thoracic vena caval-hepatic venous difference in glucose specific activity at equilibrium during i.v. infusion of [14C]glucose and hepatic blood flow, was 3·5 ± 0·8 mg/ kg/min. This was not changed by i.v. infusion of 10% ethanolic saline or cortisol in ethanolic saline, at 1 mg/kg/h for 90 min, although the cortisol infusion caused the peripheral blood glucose concentration to rise from 56·5 ± 7·3 to 83·2 ± 10·3 mg/100 ml.
The rate of metabolic clearance of glucose fell from 6·1 ± 1·1 to 4·2 ± 0·9 ml/kg/min during i.v. cortisol infusion. Daily i.m. injection of 1 mg cortisol acetate/kg for 5 days caused an increase in hepatic new glucose release to 8·0 ± 1·6 mg/kg/min.
The findings support the proposition that, in this marsupial, the short-term effect of cortisol on plasma glucose concentration is due to inhibition of peripheral glucose utilization, whereas the long-term effect is due to increased hepatic glucose production.
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The effects of injections of cortisol, corticosterone and ACTH on indices of carbohydrate, fat and protein metabolism were investigated in the conscious echidna, Tachyglossus aculeatus.
Intravenous infusion of cortisol and corticosterone for 2 h at rates of 3 and 30 μg/kg/h respectively did not cause significant changes in the plasma concentrations of glucose, urea or amino acids during a 12·5 h observation period. In contrast, a dose-related increase in plasma free fatty acid (FFA) concentration was observed. Infusion of synthetic ACTH at 2 i.u./kg/h for 2 h caused a minor, short-lived increase in FFA concentration.
Daily i.m. injections of 0·2 mg cortisol or corticosterone acetates/kg, which raised plasma total corticosteroid concentrations to levels characteristic of maximal ACTH stimulation, did not cause glycosuria nor was there any change in body weight, nitrogen intake or urinary nitrogen excretion. However, there was a minor, but significant, increase in plasma glucose concentration. The liver glycogen content of 24 h fasted, corticosteroid-treated animals was similar to that of fasted control animals.
It is concluded that cortisol, corticosterone and ACTH have only minor effects on carbohydrate and protein metabolism and that the main action of these hormones may be to mobilize fat reserves.
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The total corticosteroid concentrations in the peripheral plasma of unanaesthetized, undisturbed quokkas were 0·75 ± 0·10 (s.e.m.) and 0·93 ± 0·14 μg/100 ml in male and female quokkas respectively. Repeated sampling for periods of 36–49 h disclosed irregular fluctuations over the range 0·4–5·0 μg/100 ml, but no evidence for a regular periodicity. The major corticosteroid was usually cortisol but corticosterone contributed 25–50% of the total unstimulated corticosteroid concentration. Relatively minor concentrations of 11-deoxycortisol were detected.
Constant-rate i.v. infusion of ACTH caused a significant increase in the concentration of total corticosteroids in the plasma; this increase was detectable at a dose of 0·05 i.u. ACTH/kg/h, and rose to approximately 15 times the control value at a dose of 2·0 i.u./kg/h. This increase was due mainly to a change in the concentration of cortisol. Synthetic (β1–24) and porcine ACTH were equipotent. The sensitivity of the quokka to ACTH was approximately one-tenth that of another marsupial (Trichosurus vulpecula) or 1/160 that of man.
Moderate disturbance increased the concentration of corticosteroids in the plasma to the same level as that caused by infusion of 0·1 i.u. ACTH/kg/h, the increase being mainly in the cortisol fraction. High-affinity binding of cortisol and corticosterone by plasma proteins was demonstrated. The maximum binding capacities for cortisol were 3·89 ± 0·5 and 3·02 ± 0·6 μg/100 ml in female and male quokkas respectively. The mean association constant was 3·2 × 1081/mol at 4 °C and 5·5 × 1071/mol at 36 °C. The maximum binding capacity for corticosterone was approximately one-third that of cortisol.
