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Details are given of a technique by which the mineralocorticoid content of extracts of suprarenal cortex may be assayed in adrenalectomized dogs, with an accuracy of ±5%. The power of these extracts to maintain life in adrenalectomized animals is simultaneously tested. The results of the assay become available in 12–14 days.
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The effects of injected glycine on the liver glycogen of fasting normal and adrenalectomized mice have been compared with those of injected glucose.
In both normal mice and cortisone-treated adrenalectomized mice glycine caused significant reduction in hepatic glycogen (Table 1).
In salt-maintained and in DOCA-treated adrenalectomized mice,glycine hada glycogen-sparing action, equivalent, carbon for carbon, to that of glucose.
These observations are related to the influence of C 11 oxygenated adrenal steroids on protein metabolism.
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The pioneer work of Bush (1953) indicated that although there is great variation between species in the proportions of hydrocortisone (F) and corticosterone (B) secreted into the adrenal venous blood, the F:B ratio may be expected to remain characteristic of a species. Bush found an average F:B ratio of 4·0 for the cats of southern England.
A recent investigation (Ilett & Lockett, 1968) of the steroids secreted by the adrenals of young West Australian cats indicated an F:B ratio less than unity. However this result was obtained by visual comparison of the thin-layer chromatographic areas for F and B under u.v. light. Since other European workers (Endroczi, Telegedy & Bata, 1958) have also reported F as the major corticosteroid in the adrenal venous blood of cats, quantitative estimation has now been made of the F:B ratio in the adrenal venous blood of young and old West Australian domestic cats. Steroid
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SUMMARY
Repeated exposures of intact rats, neurohypophysectomized rats and rats with denervated kidneys to high-pitched sound (20 kcyc./sec.) for 2 sec. with an intensity of 98–100 decibels caused diuresis, natriuresis and kaluresis: the rate of urinary excretion of adrenaline rose very significantly. Adrenal demedullation abolished the natriuresis and kaluresis in response to 20 kcyc./sec. and converted the diuresis to an antidiuresis. The renal response of normal rats to 20 kcyc./sec. was therefore attributed to the release of adrenaline from the adrenal medulla in amounts sufficient to prevent an emotional release of antidiuretic hormone from the neurohypophysis. Since 20 kcyc./sec. caused a significant increase in the urinary output of vasopressin by adrenalectomized rats, an emotional release of vasopressin is assumed to have proceeded, uninhibited, in adrenal-de-medullated rats exposed to 20 kcyc./sec., and to have caused the observed antidiuresis.
The diuresis, natriuresis and kaluresis caused by 150 cyc./sec. mimicked by s.c. injection of 4 m-u. oxytocin, was unaffected by demedullation of the adrenals and was not accompanied by increase in urinary adrenaline.
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Cat kidneys perfused with heparinized blood from heart-lung circuits (Davey & Lockett, 1960; Lockett, 1966) reabsorbed 99% of the filtered water and sodium. By contrast, kidneys similarly isolated but perfused from pump-oxygenator circuits reabsorbed only 96·5% of the altered Na and 98% of the filtered water (Lockett, 1967 a). The excessive leak of Na and water from kidneys perfused from a pump-oxygenator system was corrected by insertion of a heart (perfused through the coronary arteries) into the perfusion circuit. The isolated heart released a substance into the blood stream in response to reduction in atrial filling (Lockett, 1967b); an apparently identical substance was extracted, in very small amount, from heart muscle (Lockett, 1967b; Ilett & Lockett, 1968). The physico-chemical properties of the heart substance were consistent with a steroidal structure and the renal actions were qualitatively similar to those of aldosterone but differed markedly in latency of action.
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SUMMARY
Thunderclaps, recorded and replayed, and a sound frequency of 150 cyc./sec. at 98–100 decibels increased the urinary excretion of Na+ and K+ of normal but not of neurohypophysectomized rats; 150 cyc./sec. also increased urine flow. The urinary changes induced by a sound frequency of 150 cyc./sec. closely resembled those caused by the s.c. injection of 4 m-u. oxytocin.
Adrenaline hydrochloride, 0·5–10 μg./100 g. body weight, given s.c., caused antidiuresis, and reduced urinary Na+ and K+; 40 μg. adrenaline increased urine flow, and Na+ and K+ excretion. The Na:K ratio in the urine rose as the dose of adrenaline was increased.
The effect of 5 μg. adrenaline/100 g. given s.c. to rats with denervated kidneys was much the same as that of 40 μg./100 g. in unoperated rats.
Five μg. adrenaline, given subcutaneously, completely antagonized the urinary changes induced by 4 m-u. oxytocin in normal, and adrenalectomized rats, and in animals with denervated kidneys or treated with propylthiouracil. However, the oxytocin-induced kaliuresis in neurohypophysectomized rats was not antagonized.
Vasopressin, 0·2–3·0 m-u. s.c., caused antidiuresis without changes in urinary Na+ and K+ excretion; 6·0 m-u. delayed water excretion markedly and increased urinary Na+ and K+ output.
The urinary changes induced by replayed thunder were attributable to the release of oxytocin together with a lesser amount of vasopressin. By contrast a sound frequency of 150 cyc./sec. probably released oxytocin alone.
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SUMMARY
The effect of thyroxine on the oxygen uptake of mice was abolished either by hypophysectomy or by adrenalectomy and was restored in adrenalectomized mice by very small s.c. doses of adrenaline.
Hypophysectomized and neurohypophysectomized mice failed to respond by increase in oxygen uptake to subcutaneous doses of adrenaline which were calorigenic in normal and in adrenalectomized mice. Oxytocin, 4 m-u. s.c. per mouse, restored the effect of adrenaline on the oxygen consumption of neurohypophysectomized adrenalectomized mice.
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SUMMARY
The failure of adrenalectomized mice to respond to thyroxine by an increase in oxygen uptake was not reversed by intramuscular injections of thiamine. Thiamine-deficient mice were found to be incapable of responding to thyroxine by an increase in the metabolic rate.
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SUMMARY
A concentration of 0·01 μg. (—)-triiodothyronine in the Tyrode's fluid bathing a phrenic nerve diaphragm preparation has been shown to decrease the acetylcholine appearing in the bath fluid in response to tetanus of the diaphragm through the phrenic nerve at a fixed number of impulses per sec. for a fixed number of minutes, when (a) eserine (40 μg./ml.) was used to inhibit the cholinesterase and the acetylcholine was assayed on leech muscle; and (b) prostigmine (5 × 10-6) was used as the anticholinesterase and the acetylcholine was assayed by its depressor effect on the arterial pressure of rats.
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SUMMARY
1. The adrenal glands of thiamine-deficient mice weighed more than those of normal mice and responded to adrenocorticotrophic hormone, but not to cold stress, by further hypertrophy.
2. Concomitant effects of thiamine deficiency were: (a) absence of change in pain threshold; (b) increased tolerance to intravenously injected acetylcholine; (c) increased storage of adrenaline in the adrenals; (d) decreased sensitivity of the vascular bed to noradrenaline but not to adrenaline.
3. Injections of adrenocortical extract prolonged the lives of thiamine-deficient animals exposed to a cold environment.
