Clinical experience with long-term sulfonylurea treatment has been discussed in the management of diabetes mellitus. Because of the close relationship between fasting serum insulin-like activity and the rate constant for glucose utilization (K) after glucose loading, the latter values were used for screening diabetics in place of the serum insulin-like activity, except for severe diabetics with K value below 0.04. Oral anti-diabetic drugs, such as sulfonylurea, were not effective in diabetics who had no significant extra-insulin secretion reserve. Secondary failure was found to occur more rapidly and more frequently in diabetics with low fasting serum insulin-like activity. In diabetics with low fasting serum insulin-like activity but with relatively high extra-insulin secretion, these drugs were significantly effective and secondary failure developed less rapidly.

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The three possible sites of renin formation in the kidney were investigated cytologically in rats with various blood pressure levels induced by hormonal agencies. The pre-treated control rats (1), unilaterally nephrectomized and given saline, were of normotensive status; the adrenalectomized and thyroidectomized rats (2) with the same pre-treatment showed a slight hypotension; while marked hypertension followed the administration of cortisone and thyroxine (3) and of DOCA and thyroxine (4) in pre-treated rats. In particular, DOCA and thyroxine administration resulted in most significant hypertension over 280 mm Hg. The granules in juxtaglomerular apparatus commonly much or less decreased in number, irrespective of blood pressure value. In the proximal convoluted tubules, the changes were equivocal in 1 and 3, but some signs of impairment both in 2 and 4 were not in a state of equilibrium with the blood pressure value. In the dark cells of the distal renal tubules, 1 showed no mean changes; 2 resulted in atrophy; 3 revealed hypertrophy; 4 produced the most progressive increase both in the cellvolume and cell-number, when the dark cells contained the typical intracellular canaliculus which may be concerned with the acceleration in basal secretion. It was suggested that the possible site of renin formation is the dark cell.

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1. 28-days treatment with 5mg Cortisone daily produces in guinea-pigs the wellknown atrophy of the adrenals, associated with a low nuclear volume of the fasciculata cells of the adrenal cortex and a decreased 17-OHCS excretion in urine, comparable to hypophysectomized animals. Eight to ten days after discontinuing the Cortisone treatment, during which period there is no reaction to stressful stimuli, the reduced levels increase and exceed its previous values in the so called “Rebound-phenomenon”.
2. After simultaneous treatment with 0.1mg Oestradiol-proprionate or 0.5mg Methandrostenolone respectively the adrenal atrophy can be prevented and the reaction to stress seems to occur earlier than in animals treated with Cortisone only. The 17-OHCS excretion remains low, possibly because of metabolic alterations.

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The adrenals of rat fetuses obtained from mothers whose pregnancy was prolonged by injection of progesterone were compared with those of fetuses in normal pregnancy and of neonatals, with particular reference to the weight, ascorbic acid content and histology.
During normal pregnancy, the fetal adrenal weight steadily increased up to the 21st day of pregnancy, showing an especially pronounced rise from the 20th to 21st day of pregnancy. From the 21st to 22nd day, there was no reliable in crease in fetal adrenal weight. After birth, the adrenal of neonatals was lighter and cortical cells were smaller than those in the fetal stage. Ascorbic acid content increased on the 22nd day of pregnancy, showing little fluctuation after birth. Osmiophilic materials increased in amount. When pregnancy was prolonged for 2 or 3 days, the fetal adrenals did not show atrophy, but gained weight, with a fall in ascorbic acid content. Osmiophilic materials were fewer than in the normal neonatals.
The adrenals of progesterone-treated mothers did not show any significant change, neither in weight nor in ascorbic acid content, as compared to those of the normal untreated mothers. Progesterone, when injected to the newborn rats, failed to induce a distinct alteration in adrenal weight and histology, but caused a slight decrease in ascorbic acid content.
It is concluded that the retardation of fetal adrenal growth does not occur in prolonged pregnancy.

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