Phosphorus Metabolism of the Adrenal Gland of the Rat

1956 ◽  
Vol 187 (1) ◽  
pp. 11-14 ◽  
Author(s):  
Doris Nicholls ◽  
R. J. Rossiter

Observations were made on the incorporation of inorganic phosphate labeled with P32 into the inorganic P, 20-minute hydrolyzable P and total acid-soluble P of the adrenal gland of rats either maintained at room temperature (22 ± 1°C) or conditioned to cold (3 ± 1°C). In confirmation of previous findings, there was an increase in the incorporation of inorganic P32 into the acid-soluble P of the adrenal of the rats maintained in the cold. Exposure to more severe cold (–5°C) for 2 hours, caused a great increase in the incorporation of inorganic P32 into the acid-soluble P of the adrenal of the nonacclimatized rats, compared to a slight, and statistically insignificant, increase in the acclimatized animals. The adrenal response to cold in the nonacclimatized rats was greatly decreased by the prior administration of cortisone.

1956 ◽  
Vol 34 (5) ◽  
pp. 919-926 ◽  
Author(s):  
Doris Nicholls

Brief exposure of rats to a cold environment increased the incorporation of inorganic P32 into the inorganic P, 20-min. hydrolyzable P, and total acid-soluble P of the adrenal gland. This increase was abolished by the administration of sodium ascorbate. Similar quantities of sodium succinate were without effect. The effect of ascorbate was largely due to the fact that it increased the phosphorus metabolism of the adrenals of rats maintained at room temperature. ACTH increased the incorporation of P32 into the acid-soluble P fractions of the adrenal of hypophysectomized rats. This effect of ACTH was greatly increased by sodium ascorbate. These results confirm the suggestion of Dugal that sodium ascorbate may potentiate the effect of ACTH.


1956 ◽  
Vol 34 (1) ◽  
pp. 919-926 ◽  
Author(s):  
Doris Nicholls

Brief exposure of rats to a cold environment increased the incorporation of inorganic P32 into the inorganic P, 20-min. hydrolyzable P, and total acid-soluble P of the adrenal gland. This increase was abolished by the administration of sodium ascorbate. Similar quantities of sodium succinate were without effect. The effect of ascorbate was largely due to the fact that it increased the phosphorus metabolism of the adrenals of rats maintained at room temperature. ACTH increased the incorporation of P32 into the acid-soluble P fractions of the adrenal of hypophysectomized rats. This effect of ACTH was greatly increased by sodium ascorbate. These results confirm the suggestion of Dugal that sodium ascorbate may potentiate the effect of ACTH.


1955 ◽  
Vol 33 (1) ◽  
pp. 233-247 ◽  
Author(s):  
Doris Nicholls ◽  
R. J. Rossiter

Observations were made on the effects of cold stress (3° ± 1 °C.) on the concentration of phosphorus and the incorporation of inorganic phosphate labelled with radioactive phosphorus (P32) into the following P-containing fractions in the rat: the inorganic P of the plasma, the inorganic P, 20-min. hydrolyzable P, and total acid-soluble P of the adrenal gland. With short periods of cold stress (2, 3, 6, 24 hr.) there was an increase in the relative specific activity of each of the adrenal fractions, greatest for an exposure of 2–3 hr. and least for 24 hr., with no significant change in the specific activity of the inorganic P of the plasma. With longer periods in the cold (2, 4, 8, 16 days), in addition to the usual increase in adrenal weight, there was an increase in the relative specific activity of each of the three acid-soluble P fractions of the adrenal. The increase in specific activity was not due to a decrease in the concentration of P in any of the fractions.Evidence is presented for the view that this change in the phosphorus metabolism of the adrenal can be interpreted in terms of an increase in the rate at which inorganic P32 passes across the cell membrane, i.e. from the extracellular to the cellular fluid. It is suggested that the change after a short (2–3 hr.) exposure to the cold is brought about by the stimulation of the adrenal cortex by endogenous ACTH from the pituitary. The change after longer (several days) exposures may be related to the function of the thyroid gland.


1955 ◽  
Vol 33 (3) ◽  
pp. 233-247 ◽  
Author(s):  
Doris Nicholls ◽  
R. J. Rossiter

Observations were made on the effects of cold stress (3° ± 1 °C.) on the concentration of phosphorus and the incorporation of inorganic phosphate labelled with radioactive phosphorus (P32) into the following P-containing fractions in the rat: the inorganic P of the plasma, the inorganic P, 20-min. hydrolyzable P, and total acid-soluble P of the adrenal gland. With short periods of cold stress (2, 3, 6, 24 hr.) there was an increase in the relative specific activity of each of the adrenal fractions, greatest for an exposure of 2–3 hr. and least for 24 hr., with no significant change in the specific activity of the inorganic P of the plasma. With longer periods in the cold (2, 4, 8, 16 days), in addition to the usual increase in adrenal weight, there was an increase in the relative specific activity of each of the three acid-soluble P fractions of the adrenal. The increase in specific activity was not due to a decrease in the concentration of P in any of the fractions.Evidence is presented for the view that this change in the phosphorus metabolism of the adrenal can be interpreted in terms of an increase in the rate at which inorganic P32 passes across the cell membrane, i.e. from the extracellular to the cellular fluid. It is suggested that the change after a short (2–3 hr.) exposure to the cold is brought about by the stimulation of the adrenal cortex by endogenous ACTH from the pituitary. The change after longer (several days) exposures may be related to the function of the thyroid gland.


1959 ◽  
Vol 37 (5) ◽  
pp. 661-670 ◽  
Author(s):  
Rosemary Molloy ◽  
Doris Nicholls ◽  
William Farrington ◽  
R. J. Rossiter

Further observations are described on the measurement of the incorporation of inorganic phosphate labelled with P32 into the inorganic phosphate of the adrenal gland to assess the immediate pituitary–adrenal response when cold acclimatized and non-acclimatized rats are exposed to more severe cold (2 hours at −5 °C). In rats acclimatized to cold by conditioning to 3 °C for 4 weeks, this immediate pituitary–adrenal response was considerably less than that in non-acclimatized rats maintained at room temperature (22 °C). The reduction in the immediate pituitary–adrenal response took 3 to 4 weeks to develop and persisted for 12 hours, but not for 4 days. Rats that were conditioned to −5 °C by exposures for 2 or 6 hours daily for 4 weeks showed no reduction in the immediate pituitary–adrenal response to more severe cold, but there was a significant decrease in this response in rats conditioned for 6 hours daily for 8 weeks.Rats acclimatized to cold by conditioning to 3 °C for 4 weeks showed greater survival when exposed to an environmental temperature of −15 °C than rats conditioned to 22 °C. Rats that were conditioned to −5 °C for brief daily periods (2 hours or 6 hours) for 4 weeks or 8 weeks also survived exposure to severe cold (−22 °C) better than rats maintained at room temperature.In general, significant increases in adrenal weight were found in those cold-conditioned rats that showed a reduced pituitary–adrenal response. However, it is concluded that the development of increased survival on exposure to severe cold, by a process of conditioning to less severe cold, is not necessarily accompanied by a reduction in the immediate pituitary–adrenal response to severe cold, or by an increase in weight of the adrenal glands.


1959 ◽  
Vol 37 (1) ◽  
pp. 661-670
Author(s):  
Rosemary Molloy ◽  
Doris Nicholls ◽  
William Farrington ◽  
R. J. Rossiter

Further observations are described on the measurement of the incorporation of inorganic phosphate labelled with P32 into the inorganic phosphate of the adrenal gland to assess the immediate pituitary–adrenal response when cold acclimatized and non-acclimatized rats are exposed to more severe cold (2 hours at −5 °C). In rats acclimatized to cold by conditioning to 3 °C for 4 weeks, this immediate pituitary–adrenal response was considerably less than that in non-acclimatized rats maintained at room temperature (22 °C). The reduction in the immediate pituitary–adrenal response took 3 to 4 weeks to develop and persisted for 12 hours, but not for 4 days. Rats that were conditioned to −5 °C by exposures for 2 or 6 hours daily for 4 weeks showed no reduction in the immediate pituitary–adrenal response to more severe cold, but there was a significant decrease in this response in rats conditioned for 6 hours daily for 8 weeks.Rats acclimatized to cold by conditioning to 3 °C for 4 weeks showed greater survival when exposed to an environmental temperature of −15 °C than rats conditioned to 22 °C. Rats that were conditioned to −5 °C for brief daily periods (2 hours or 6 hours) for 4 weeks or 8 weeks also survived exposure to severe cold (−22 °C) better than rats maintained at room temperature.In general, significant increases in adrenal weight were found in those cold-conditioned rats that showed a reduced pituitary–adrenal response. However, it is concluded that the development of increased survival on exposure to severe cold, by a process of conditioning to less severe cold, is not necessarily accompanied by a reduction in the immediate pituitary–adrenal response to severe cold, or by an increase in weight of the adrenal glands.


1956 ◽  
Vol 34 (1) ◽  
pp. 543-553
Author(s):  
Doris Nicholls ◽  
F. C. Heagy ◽  
R. J. Rossiter

The incorporation of inorganic phosphate labelled with P32 into the lipid P and ribonucleotide P of the adrenal glands of rats exposed to cold (3 ± 1 °C.) for eight days was measured 16 hr. after the P32 injection. In the cold-exposed animals, there was a decrease in the specific activity of both the lipid P and the ribonucleotide P and also a decrease in the specific activity of the lipid P and the ribonucleotide P relative to that of the inorganic P of the adrenal. The cold exposure caused an increase in the amounts of lipid P, ribonucleic acid (RNA), and desoxyribonucleic acid (DNA) per pair of adrenals. There was an increase in the ratio lipid P: DNA-P, but no change in the ratio RNA-P: DNA-P. Calculation showed that the cold exposure caused a decrease in the percentage renewal rate of both lipid P and ribonucleotide P, most of which could be attributed to the increased amounts of lipid P and ribonucleotide P present at the beginning of the isotope experiment. However, when allowance for this was made by calculating the renewal rates of the P of the phospholipid and RNA per pair of adrenals, the values remained slightly less in the cold-exposed animals.


1956 ◽  
Vol 34 (3) ◽  
pp. 543-553 ◽  
Author(s):  
Doris Nicholls ◽  
F. C. Heagy ◽  
R. J. Rossiter

The incorporation of inorganic phosphate labelled with P32 into the lipid P and ribonucleotide P of the adrenal glands of rats exposed to cold (3 ± 1 °C.) for eight days was measured 16 hr. after the P32 injection. In the cold-exposed animals, there was a decrease in the specific activity of both the lipid P and the ribonucleotide P and also a decrease in the specific activity of the lipid P and the ribonucleotide P relative to that of the inorganic P of the adrenal. The cold exposure caused an increase in the amounts of lipid P, ribonucleic acid (RNA), and desoxyribonucleic acid (DNA) per pair of adrenals. There was an increase in the ratio lipid P: DNA-P, but no change in the ratio RNA-P: DNA-P. Calculation showed that the cold exposure caused a decrease in the percentage renewal rate of both lipid P and ribonucleotide P, most of which could be attributed to the increased amounts of lipid P and ribonucleotide P present at the beginning of the isotope experiment. However, when allowance for this was made by calculating the renewal rates of the P of the phospholipid and RNA per pair of adrenals, the values remained slightly less in the cold-exposed animals.


1959 ◽  
Vol 37 (1) ◽  
pp. 671-677
Author(s):  
Doris Nicholls ◽  
Rosemary Molloy ◽  
Kathleen Stavraky ◽  
R. J. Rossiter

The incorporation of inorganic phosphorus labelled with P32 into the inorganic phosphorus of the adrenal gland was measured in rats acclimatized to cold for 4 weeks. Previously it was reported that the immediate pituitary–adrenal response to brief cold exposure (2 hours at −5 °C), as judged by the increased P32 incorporation is considerably decreased in rats that have been acclimatized. Some observations are now reported on the mechanism of this reduced immediate response.The administration of ACTH, pitressin, or adrenaline caused similar increases in the adrenal phosphorus metabolism in acclimatized and non-acclimatized control rats. Acclimatization could still be demonstrated in rats after the fur had been removed by clipping.From these results it is concluded that the decreased immediate pituitary–adrenal response to an exposure to more severe cold, observed in acclimatized rats, is not the result of an increased fur thickness, nor is it the result of a decreased sensitivity of the adrenal tissue to ACTH, or to a decreased sensitivity of the pituitary or hypothalamus to a given stimulus. It is suggested that the reduction in the immediate pituitary–adrenal response to a more severe cold stress in acclimatized rats might be due to an alteration in the sensitivity of the peripheral nerve receptors, or in the mechanism, nervous or otherwise, whereby the pituitary is stimulated.


1954 ◽  
Vol 32 (3) ◽  
pp. 261-270 ◽  
Author(s):  
B. E. Riedel ◽  
R. J. Rossiter

The specific activity of the intracellular inorganic phosphate (P) of the adrenal gland relative to that of the inorganic P of the plasma is significantly decreased in hypophysectomized rats at time intervals as long as 16 hr. after the injection of inorganic P labelled with P32. The specific activity of the intracellular inorganic P was determined (1) by measuring the specific activity of the easily-hydrolyzable acid-soluble P, which rapidly comes into isotope equilibrium with the intracellular inorganic P, (2) by calculation, from the specific activity of the inorganic P of the whole adrenal, assuming values for the specific activity and the concentration of the inorganic P of the extracellular fluid and the volume of the extracellular fluid compartment, and (3) by measuring the specific activities of the inorganic P of both the adrenal gland and the plasma at a series of time intervals after the injection of the P32. It is concluded that the decrease in the relative specific activity of the intracellular inorganic P of the adrenal is the result of a slowing in the passage of inorganic P32 across the cell membrane, i.e. from the extracellular to the intracellular fluid.


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