The potassium content of incubated rat adrenal tissue is significantly higher when calcium is present in the incubation medium than when it is absent. The effect of calcium on the sodium content of the adrenal depends upon the presence of ACTH; increased values are obtained with calcium in the presence of ACTH, decreased values in its absence. There is no correlation between the potassium or sodium content of the tissue and its ability to respond to ACTH. Adenosine 3′,5′-monophosphate triples the steroid output of incubated adrenal glands in the absence of both glucose and calcium. Addition of calcium further doubles this response while glucose has only a small effect. The stimulation of steroid production following short contact with ACTH does not depend upon the presence of calcium or glucose in the medium during the time the glands are exposed to the hormone. The results suggest that some step between contact of the tissue with ACTH and the elaboration of adenosine 3′,5′-monophosphate requires the presence of glucose and not necessarily calcium and that a reaction in the sequence between elaboration of the nucleotide and steroid production requires the presence of calcium, but not of glucose.

The potassium content of incubated rat adrenal tissue is significantly higher when calcium is present in the incubation medium than when it is absent. The effect of calcium on the sodium content of the adrenal depends upon the presence of ACTH; increased values are obtained with calcium in the presence of ACTH, decreased values in its absence. There is no correlation between the potassium or sodium content of the tissue and its ability to respond to ACTH. Adenosine 3′,5′-monophosphate triples the steroid output of incubated adrenal glands in the absence of both glucose and calcium. Addition of calcium further doubles this response while glucose has only a small effect. The stimulation of steroid production following short contact with ACTH does not depend upon the presence of calcium or glucose in the medium during the time the glands are exposed to the hormone. The results suggest that some step between contact of the tissue with ACTH and the elaboration of adenosine 3′,5′-monophosphate requires the presence of glucose and not necessarily calcium and that a reaction in the sequence between elaboration of the nucleotide and steroid production requires the presence of calcium, but not of glucose.

The pharmacokinetics of lorazepam was examined in 10 male patients with insulin-dependent diabetes mellitus before and following treatment with neomycin and cholestyramine. Neomycin and cholestyramine were given in an attempt to block the enterohepatic circulation of lorazepam and so to permit an in vivo estimate of hepatic glucuronidation. The volume of distribution and clearance of free lorazepam in diabetic patients were not significantly different from the corresponding estimates in 14 normal controls. Neomycin and cholestyramine increased the clearance of lorazepam by 63% consistent with their effect in non-diabetic controls. However, patients on beef/pork insulin exhibited a greater than normal increase on this interupting regimen (125%), and had a significantly greater neomycin/cholestyramine cycling-interrupted clearance of lorazepam than either normal controls or patients on human insulin (15.4 vs. 6.96 and 7.87 ml.min-1.kg-1). The clearance was correlated positively and significantly with HbA1c and glycated proteins (fructosamine), but only in patients on human insulin. Thus, the pharmacokinetics of lorazepam was not altered in patients with insulin-dependent diabetes mellitus. However, it is possible that there are differences in the rate and extent of hepatic glucuronidation and enterohepatic circulation of lorazepam between patients treated with beef/pork and human insulins and between diabetics treated with beef/pork insulin and non-diabetic controls.